See J. P. A. Rémusat,Histoire de la ville de Khotan(Paris, 1820); and Sven Hedin,Through Asia(Eng. trans., London, 1898), chs. lx. and lxii., andScientific Results of a Journey in Central Asia, 1899-1902, vol. ii. (Stockholm, 1906).
See J. P. A. Rémusat,Histoire de la ville de Khotan(Paris, 1820); and Sven Hedin,Through Asia(Eng. trans., London, 1898), chs. lx. and lxii., andScientific Results of a Journey in Central Asia, 1899-1902, vol. ii. (Stockholm, 1906).
(J. T. Be.)
1Sir H. Yule,The Book of Ser Marco Polo, bk. i. ch. xxxvi. (3rd ed., London, 1903).
1Sir H. Yule,The Book of Ser Marco Polo, bk. i. ch. xxxvi. (3rd ed., London, 1903).
KHOTIN,orKhoteen(variously written Khochim, Choczim, and Chocim), a fortified town of South Russia, in the government of Bessarabia, in 48° 30′ N. and 26° 30′ E., on the right bank of the Dniester, near the Austrian (Galician) frontier, and opposite Podolian Kamenets. Pop. (1897), 18,126. It possesses a few manufactures (leather, candles, beer, shoes, bricks), and carries on a considerable trade, but has always been of importance mainly as a military post, defending one of the most frequented passages of the Dniester. In the middle ages it was the seat of a Genoese colony; and it has been in Polish, Turkish and Austrian possession. The chief events in its annals are the defeat of the Turks in 1621 by Ladislaus IV., of Poland, in 1673 by John Sobieski, of Poland, and in 1739 by the Russians under Münnich; the defeat of the Russians by the Turks in 1768; the capture by the Russians in 1769, and by the Austrians in 1788; and the occupation by the Russians in 1806. It finally passed to Russia with Bessarabia in 1812 by the peace of Bucharest.
KHULNA,a town and district of British India, in the Presidency division of Bengal. The town stands on the river Bhairab, and is the terminus of the Bengal Central railway, 109 m. E. of Calcutta. Pop. (1901), 10,426. It is the most important centre of river-borne trade in the delta.
TheDistrict of Khulnalies in the middle of the delta of the Ganges, including a portion of the Sundarbans or seaward fringe of swamps. It was formed out of Jessore in 1882. Area (excluding the Sundarbans), 2077 sq. m. Besides the Sundarbans, the north-east part of the district is swampy; the north-west is more elevated and drier, while the central part, though low-lying, is cultivated. The whole is alluvial. In 1901 the population was 1,253,043, showing an increase of 6% in the decade. Rice is the principal crop; mustard, jute and tobacco are also grown, and the fisheries are important. Sugar is manufactured from the date palm. The district is entered by the Bengal Central railway, but by far the greater part of the traffic is carried by water.
SeeDistrict Gazetteer(Calcutta, 1908).
SeeDistrict Gazetteer(Calcutta, 1908).
KHUNSAR,a town of Persia, sometimes belonging to the province of Isfahan, at others to Irak, 96 m. N.W. of Isfahan, in 33° 9′ N., 50° 23′ E., at an elevation of 7600 ft. Pop., about 10,000. It is picturesquely situated on both sides of a narrow valley through which the Khunsar River, a stream about 12 ft. wide, flows in a north-east direction to Kuom. The town and its fine gardens and orchards straggle some 6 m. along the valley with a mean breadth of scarcely half a mile. There is a great profusion of fruit, the apples yielding a kind of cider which, however, does not keep longer than a month. The climate is cool in summer and cold in winter. There are five caravanserais, three mosques and a post office.
KHURJA,a town of British India, in the Bulandshahr district of the United Provinces, 27 m. N.W. of Aligarh, near the mainline of the East Indian railway. Pop. (1901), 29,277. It is an important centre of trade in grain, indigo, sugar andghi, and has cotton gins and presses and a manufacture of pottery. Jain traders form a large and wealthy class; and the principal building in the town is a modern Jain temple, a fine domed structure richly carved and ornamented in gold and colours.
KHYBER PASS,the most important of the passes which lead from Afghanistan into India. It is a narrow defile winding between cliffs of shale and limestone 600 to 1000 ft. high, stretching up to more lofty mountains behind. No other pass in the world has possessed such strategic importance or retains so many historic associations as this gateway to the plains of India. It has probably seen Persian and Greek, Seljuk, Tatar, Mongol and Durani conquerors, with the hosts of Alexander the Great, Mahmud of Ghazni, Jenghiz Khan, Timur, Baber, Nadir Shah, Ahmed Shah, and numerous other warrior chiefs pass and repass through its rocky defiles during a period of 2000 years. The mountain barrier which separates the Peshawar plains from the Afghan highlands differs in many respects from the mountain barrier which intervenes between the Indus plains and the plateau farther south. To the south this barrier consists of a series of flexures folded parallel to the river, through which the plateau drainage breaks down in transverse lines forming gorges and clefts as it cuts through successive ridges. West of Peshawar the strike of the mountain systems is roughly from west to east, and this formation is maintained with more or less regularity as far south as the Tochi River and Waziristan. Almost immediately west of Peshawar, and stretching along the same parallel of latitude from the meridian of Kabul to within ten miles of the Peshawar cantonment, is the great central range of the Safed Koh, which forms throughout its long, straight line of rugged peaks the southern wall, or water-divide, of the Kabul River basin. About the meridian of 71 E. it forks, sending off to the north-east what is locally known as a spur to the Kabul River, but which is geographically only part of that stupendous water-divide which hedges in the Kunar and Chitral valleys, and, under the name of the Shandur Range, unites with the Hindu Kush near the head of the Taghdumbash Pamir. The Kabul River breaks through this northern spur of the Safed Koh; and in breaking through it is forced to the northward in a curved channel or trough, deeply sunk in the mountains between terrific cliffs and precipices, where its narrow waterway affords no foothold to man or beast for many miles. To reach the Kabul River within Afghan territory it is necessary to pass over this water-divide; and the Khyber stream, flowing down from the pass at Landi Kotal to a point in the plains opposite Jamrud, 9 m. W. of Peshawar, affords the opportunity.
Pursuing the main road from Peshawar to Kabul, the fort of Jamrud, which commands the British end of the Khyber Pass, lies some 11 m. W. of Peshawar. The road leads through a barren stony plain, cut up by water-courses and infested by all the worst cut-throats in the Peshawar district. Some three miles beyond Jamrud the road enters the mountains at an opening called Shadi Bagiar, and here the Khyber proper begins. The highway runs for a short distance through the bed of a ravine, and then joins the road made by Colonel Mackeson in 1839-1842, until it ascends on the left-hand side to a plateau called Shagai. From here can be seen the fort of Ali Masjid, which commands the centre of the pass, and which has been the scene of more than one famous siege. Still going westward the road turns to the right, and by an easy zigzag descends to the river of Ali Masjid, and runs along its bank. The new road along this cliff was made by the British during the Second Afghan War (1879-80), and here is the narrowest part of the Khyber, not more than 15 ft. broad, with the Rhotas hill on the right fully 2000 ft. overhead. Some three miles farther on the valley widens, and on either side lie the hamlets and some sixty towers of the Zakka Khel Afridis. Then comes the Loargi Shinwari plateau, some seven miles in length and three in its widest part, ending at Landi Kotal, where is another British fort, which closes this end of the Khyber and overlooks the plains of Afghanistan. After leaving Landi Kotal the great Kabul highway passes between low hills, until it debouches on the Kabul River and leads to Dakka. The whole of the Khyber Pass from end to end lies within the country of the Afridis, and is now recognized as under British control. From Shadi Bagiar on the east to Landi Kotal on the west is about 20 m. in a straight line.
The Khyber has been adopted by the British as the main road to Kabul, but its difficulties (before they were overcome by British engineers) were such that it was never so regarded by former rulers of India. The old road to India left the Kabul River near its junction with the Kunar, and crossed the great divide between the Kunar valley and Bajour; then it turned southwards to the plains. During the first Afghan War the Khyber was the scene of many skirmishes with the Afridis and some disasters to the British troops. In July 1839 Colonel Wade captured the fortress of Ali Masjid. In 1842, when Jalalabad was blockaded, Colonel Moseley was sent to occupy the same fort, but was compelled to evacuate it after a few days owing to scarcity of provisions. In April of the same year it was reoccupied by General Pollock in his advance to Kabul. It was at Ali Masjid that Sir Neville Chamberlain’s friendly mission to the amir Shere Ali was stopped in 1878, thus causing the second Afghan War; and on the outbreak of that war Ali Masjid was captured by Sir Samuel Browne. The treaty which closed the war in May 1879 left the Khyber tribes under British control. From that time the pass was protected by jezailchis drawn from the Afridi tribe, who were paid a subsidy by the British government. For 18 years, from 1879 onward, Colonel R. Warburton controlled the Khyber, and for the greater part of that time secured its safety; but his term of office came to an end synchronously with the wave of fanaticism which swept along the north-west border of India during 1897. The Afridis were persuaded by their mullahs to attack the pass, which they themselves had guaranteed. The British government were warned of the intended movement, but only withdrew the British officers belonging to the Khyber Rifles, and left the pass to its fate. The Khyber Rifles, deserted by their officers, made a half-hearted resistance to their fellow-tribesmen, and the pass fell into the hands of the Afridis, and remained in their possession for some months. This was the chief cause of the Tirah Expedition of 1897. The Khyber Rifles were afterwards strengthened, and divided into two battalions commanded by four British officers.
SeeEighteen Years in the Khyber, by Sir Robert Warburton (1900);Indian Borderland, by Sir T. Holdich (1901).
SeeEighteen Years in the Khyber, by Sir Robert Warburton (1900);Indian Borderland, by Sir T. Holdich (1901).
(T. H. H.*)
KIAKHTA,a town of Siberia, one of the chief centres of trade between Russia and China, on the Kiakhta, an affluent of the Selenga, and on an elevated plain surrounded by mountains, in the Russian government of Transbaikalia, 320 m. S.W. of Chita, the capital, and close to the Chinese frontier, in 50° 20′ N., 106° 40′ E. Besides the lower town or Kiakhta proper, the municipal jurisdiction comprises the fortified upper town of Troitskosavsk, about 2 m. N., and the settlement of Ust-Kiakhta, 10 m. farther distant. The lower town stands directly opposite to the Chinese emporium of Maimachin, is surrounded by walls, and consists principally of one broad street and a large exchange courtyard. From 1689 to 1727 the trade of Kiakhta was a government monopoly, but in the latter year it was thrown open to private merchants, and continued to improve until 1860, when the right of commercial intercourse was extended along the whole Russian-Chinese frontier. The annual December fairs for which Kiakhta was formerly famous, and also the regular traffic passing through the town, have considerably fallen off since that date. The Russians exchange here leather, sheepskins, furs, horns, woollen cloths, coarse linens and cattle for teas (in value 95% of the entire imports), porcelain, rhubarb, manufactured silks, nankeens and other Chinese produce. The population, including Ust-Kiakhta (5000) and Troitskosavsk (9213 in 1897), is nearly 20,000.
KIANG-SI,an eastern province of China, bounded N. by Hu-peh and Ngan-hui, S. by Kwang-tung, E. by Fu-kien, andW. by Hu-nan. It has an area of 72,176 sq. m., and a population returned at 22,000,000. It is divided into fourteen prefectures. The provincial capital is Nan-ch’ang Fu, on the Kan Kiang, about 35 m. from the Po-yang Lake. The whole province is traversed in a south-westerly and north-easterly direction by the Nan-shan ranges. The largest river is the Kan Kiang, which rises in the mountains in the south of the province and flows north-east to the Po-yang Lake. It was over the Meiling Pass and down this river that, in old days, embassies landing at Canton proceeded to Peking. During the summer time it has water of sufficient depth for steamers of light draft as far as Nan-ch’ang, and it is navigable by native craft for a considerable distance beyond that city. Another river of note is the Chang Kiang, which has its source in the province of Ngan-hui and flows into the Po-yang Lake, connecting in its course the Wu-yuen district, whence come the celebrated “Moyune” green teas, and the city of King-te-chên, celebrated for its pottery, with Jao-chow Fu on the lake. The black “Kaisow” teas are brought from the Ho-kow district, where they are grown, down the river Kin to Juy-hung on the lake, and the Siu-ho connects by a navigable stream I-ning Chow, in the neighbourhood of which city the best black teas of this part of China are produced, with Wu-ching, the principal mart of trade on the lake. The principal products of the province are tea, China ware, grass-cloth, hemp, paper, tobacco and tallow. Kiu-kiang, the treaty port of the province, opened to foreign trade in 1861, is on the Yangtsze-kiang, a short distance above the junction of the Po-yang Lake with that river.
KIANG-SU,a maritime province of China, bounded N. by Shantung, S. by Cheh-kiang, W. by Ngan-hui, and E. by the sea. It has an area of 45,000 sq. m., and a population estimated at 21,000,000. Kiang-su forms part of the great plain of northern China. There are no mountains within its limits, and few hills. It is watered as no other province in China is watered. The Grand Canal runs through it from south to north; the Yangtsze-kiang crosses its southern portion from west to east; it possesses several lakes, of which the T’ai-hu is the most noteworthy, and numberless streams connect the canal with the sea. Its coast is studded with low islands and sandbanks, the results of the deposits brought down by the Hwang-ho. Kiang-su is rich in places of interest. Nanking, “the Southern Capital,” was the seat of the Chinese court until the beginning of the 15th century, and it was the headquarters of the T’ai-p’ing rebels from 1853, when they took the city by assault, to 1864, when its garrison yielded to Colonel Gordon’s army. Hang-chow Fu and Su-chow Fu, situated on the T’ai-hu, are reckoned the most beautiful cities in China. “Above there is Paradise, below are Su and Hang,” says a Chinese proverb. Shang-hai is the chief port in the province. In 1909 it was connected by railway (270 m. long) via Su-Chow and Chin-kiang with Nanking. Tea and silk are the principal articles of commerce produced in Kiang-su, and next in importance are cotton, sugar and medicines. The silk manufactured in the looms of Su-chow is famous all over the empire. In the mountains near Nanking, coal, plumbago, iron ore and marble are found. Shang-hai, Chin-kiang, Nanking and Su-chow are the treaty ports of the province.
KIAOCHOW BAY,a large inlet on the south side of the promontory of Shantung, in China. It was seized in November 1897 by the German fleet, nominally to secure reparation for the murder of two German missionaries in the province of Shantung. In the negotiations which followed, it was arranged that the bay and the land on both sides of the entrance within certain defined lines should be leased to Germany for 99 years. During the continuance of the lease Germany exercises all the rights of territorial sovereignty, including the right to erect fortifications. The area leased is about 117 sq. m., and over a further area, comprising a zone of some 32 m., measured from any point on the shore of the bay, the Chinese government may not issue any ordinances without the consent of Germany. The native population in the ceded area is about 60,000. The German government in 1899 declared Kiaochow a free port. By arrangement with the Chinese government a branch of the Imperial maritime customs has been established there for the collection of duties upon goods coming from or going to the interior, in accordance with the general treaty tariff. Trade centres at Ts’ingtao, a town within the bay. The country in the neighbourhood is mountainous and bare, but the lowlands are well cultivated. Ts’ingtao is connected by railway with Chinan Fu, the capital of the province; a continuation of the same line provides for a junction with the main Lu-Han (Peking-Hankow) railway. The value of the trade of the port during 1904 was £2,712,145 (£1,808,113 imports and £904,032 exports).
KICKAPOO(“he moves about”), the name of a tribe of North American Indians of Algonquian stock. When first met by the French they were in central Wisconsin. They subsequently removed to the Ohio valley. They fought on the English side in the War of Independence and that of 1812. In 1852 a large band went to Texas and Mexico and gave much trouble to the settlers; but in 1873 the bulk of the tribe was settled on its present reservation in Oklahoma. They number some 800, of whom about a third are still in Mexico.
KIDD, JOHN(1775-1851), English physician, chemist and geologist, born at Westminster on the 10th of September 1775, was the son of a naval officer, Captain John Kidd. He was educated at Bury St Edmunds and Westminster, and afterwards at Christ Church, Oxford, where he graduated B.A. in 1797 (M.D. in 1804). He also studied at Guy’s Hospital, London (1797-1801), where he was a pupil of Sir Astley Cooper. He became reader in chemistry at Oxford in 1801, and in 1803 was elected the first Aldrichian professor of chemistry. He then voluntarily gave courses of lectures on mineralogy and geology: these were delivered in the dark chambers under the Ashmolean Museum, and there J. J. and W. D. Conybeare, W. Buckland, C. G. B. Daubeny and others gained their first lessons in geology. Kidd was a popular and instructive lecturer, and through his efforts the geological chair, first held by Buckland, was established. In 1818 he became a F.R.C.P.; in 1822 regius professor of medicine in succession to Sir Christopher Pegge; and in 1834 he was appointed keeper of the Radcliffe Library. He delivered the Harveian oration before the Royal College of Physicians in 1834. He died at Oxford on the 7th of September 1851.
Publications.—Outlines of Mineralogy(2 vols., 1809);A Geological Essay on the Imperfect Evidence in Support of a Theory of the Earth(1815);On the Adaptation of External Nature to the Physical Condition of Man, 1833 (Bridgewater Treatise).
Publications.—Outlines of Mineralogy(2 vols., 1809);A Geological Essay on the Imperfect Evidence in Support of a Theory of the Earth(1815);On the Adaptation of External Nature to the Physical Condition of Man, 1833 (Bridgewater Treatise).
KIDD, THOMAS(1770-1850), English classical scholar and schoolmaster, was born in Yorkshire. He was educated at Giggleswick School and Trinity College, Cambridge. He held numerous scholastic and clerical appointments, the last being the rectory of Croxton, near Cambridge, where he died on the 27th of August 1850. Kidd was an intimate friend of Porson and Charles Burney the younger. He contributed largely to periodicals, chiefly on classical subjects, but his reputation mainly rests upon his editions of the works of other scholars:Opuscula Ruhnkeniana(1807), the minor works of the great Dutch scholar David Ruhnken;Miscellanea Criticaof Richard Dawes (2nd ed., 1827);Tracts and Miscellaneous Criticismsof Richard Porson (1815). He also published an edition of the works of Horace (1817) based upon Bentley’s recension.
KIDD, WILLIAM[Captain Kidd] (c.1645-1701), privateer and pirate, was born, perhaps, in Greenock, Scotland, but his origin is quite obscure. He told Paul Lorraine, the ordinary of Newgate, that he was “about 56” at the time of his condemnation for piracy in 1701. In 1691 an award from the council of New York of £150 was given him for his services during the disturbances in the colony after the revolution of 1688. He was commissioned later to chase a hostile privateer off the coast, is described as an owner of ships, and is known to have served with credit against the French in the West Indies. In 1695 he came to London with a sloop of his own to trade. Colonel R. Livingston (1654-1724), a well-known New York landowner, recommended him to the newly appointed colonial governor Lord Bellomont, as a fit man to command a vessel to cruise against the pirates in the Eastern seas (seePirate).Accordingly the “Adventure Galley,” a vessel of 30 guns and 275 tons, was privately fitted out, and the command given to Captain Kidd, who received the king’s commission to arrest and bring to trial all pirates, and a commission of reprisals against the French. Kidd sailed from Plymouth in May 1696 for New York, where he filled up his crew, and in 1697 reached Madagascar, the pirates’ principal rendezvous. He made no effort whatever to hunt them down. On the contrary he associated himself with a notorious pirate named Culliford. The fact would seem to be that Kidd meant only to capture French ships. When he found none he captured native trading vessels, under pretence that they were provided with French passes and were fair prize, and he plundered on the coast of Malabar. During 1698-1699 complaints reached the British government as to the character of his proceedings. Lord Bellomont was instructed to apprehend him if he should return to America. Kidd deserted the “Adventure” in Madagascar, and sailed for America in one of his prizes, the “Quedah Merchant,” which he also left in the West Indies. He reached New England in a small sloop with several of his crew and wrote to Bellomont, professing his ability to justify himself and sending the governor booty. He was arrested in July 1699, was sent to England and tried, first for the murder of one of his crew, and then with others for piracy. He was found guilty on both charges, and hanged at Execution Dock, London, on the 23rd of May 1701. The evidence against him was that of two members of his crew, the surgeon and a sailor who turned king’s evidence, but no other witnesses could be got in such circumstances, as the judge told him when he protested. “Captain Kidd’s Treasure” has been sought by various expeditions and about £14,000 was recovered from Kidd’s ship and from Gardiner’s Island (off the E. end of Long Island); but its magnitude was palpably exaggerated. He left a wife and child at New York. The so-called ballad about him is a poor imitation of the authentic chant of Admiral Benbow.
Much has been written about Kidd, less because of the intrinsic interest of his career than because the agreement made with him by Bellomont was the subject of violent political controversy. The best popular account is inAn Historical Sketch of Robin Hood and Captain Kiddby W. W. Campbell (New York, 1853), in which the essential documents are quoted. But seePirate.
Much has been written about Kidd, less because of the intrinsic interest of his career than because the agreement made with him by Bellomont was the subject of violent political controversy. The best popular account is inAn Historical Sketch of Robin Hood and Captain Kiddby W. W. Campbell (New York, 1853), in which the essential documents are quoted. But seePirate.
KIDDERMINSTER,a market town and municipal and parliamentary borough of Worcestershire, England, 135½ m. N.W. by W. from London and 15 m. N. of Worcester by the Great Western railway, on the river Stour and the Staffordshire and Worcestershire canal. Pop. (1901), 24,692. The parish church of All Saints, well placed above the river, is a fine Early English and Decorated building, with Perpendicular additions. Of other buildings the principal are the town hall (1876), the corporation buildings, and the school of science and art and free library. There is a free grammar school founded in 1637. A public recreation ground, Brinton Park, was opened in 1887. Richard Baxter, who was elected by the townsfolk as their minister in 1641, was instrumental in saving the town from a reputation of ignorance and depravity caused by the laxity of their clergy. He is commemorated by a statue, as is Sir Rowland Hill, the introducer of penny postage, who was born here in 1795. Kidderminster is chiefly celebrated for its carpets. The permanency of colour by which they are distinguished is attributed to the properties of the water of the Stour, which is impregnated with iron and fuller’s earth. Worsted spinning and dyeing are also carried on, and there are iron foundries, tinplate works, breweries, malthouses, &c. The parliamentary borough returns one member. The town is governed by a mayor, 6 aldermen and 18 councillors. Area, 1214 acres.
In 736 lands upon the river Stour, called Stour in Usmere, which have been identified with the site of Kidderminster (Chideminstre), were given to Earl Cyneberght by King Æthelbald to found a monastery. If this monastery was ever built, it was afterwards annexed to the church of Worcester, and the lands on the Stour formed part of the gift of Coenwulf, king of the Mercians, to Deneberht, bishop of Worcester, but were exchanged with the same king in 816 for other property. At the Domesday Survey, Kidderminster was still in the hands of the king and remained a royal manor until Henry II. granted it to Manser Biset. The poet Edmund Waller was one of the 17th century lords of the manor. The town was possibly a borough in 1187 when the men paid £4 to an aid. As a royal possession it appears to have enjoyed various privileges in the 12th century, among them the right of choosing a bailiff to collect the toll and render it to the king, and to elect six burgesses and send them to the view of frankpledge twice a year. The first charter of incorporation, granted in 1636, appointed a bailiff and 12 capital burgesses forming a common council. The town was governed under this charter until the Municipal Reform Act of 1835. Kidderminster sent two members to the parliament of 1295, but was not again represented until the privilege of sending one member was conferred by the Reform Act of 1832. The first mention of the cloth trade for which Kidderminster was formerly noted occurs in 1334, when it was enacted that no one should make woollen cloth in the borough without the bailiff’s seal. At the end of the 18th century the trade was still important, but it began to decline after the invention of machinery, probably owing to the poverty of the manufacturers. The manufacture of woollen goods was however replaced by that of carpets, introduced in 1735. At first only the “Kidderminster” carpets were made, but in 1749 a Brussels loom was set up in the town and Brussels carpets were soon produced in large quantities.
SeeVictoria County History: Worcestershire; J. R. Burton,A History of Kidderminster, with Short Accounts of some Neighbouring Parishes(1890).
SeeVictoria County History: Worcestershire; J. R. Burton,A History of Kidderminster, with Short Accounts of some Neighbouring Parishes(1890).
KIDNAPPING(fromkid, a slang term for a child, andnapornab, to steal), originally the stealing and carrying away of children and others to serve as servants or labourers in the American plantations; it was defined by Blackstone as the forcible abduction or stealing away of a man, woman or child from their own country and sending them into another. The difference between kidnapping, abduction (q.v.) and false imprisonment is not very great; indeed, kidnapping may be said to be a form of assault and false imprisonment, aggravated by the carrying of the person to some other place. The term is, however, more commonly applied in England to the offence of taking away children from the possession of their parents. By the Offences against the Person Act 1861, “whosoever shall unlawfully, by force or fraud, lead or take away or decoy or entice away or detain any child under the age of fourteen years with intent to deprive any parent, guardian or other person having the lawful care or charge of such child of the possession of such child, or with intent to steal any article upon or about the person of such child, to whomsoever such article may belong, and whosoever shall with any such intent receive or harbour any such child, &c.,” shall be guilty of felony, and is liable to penal servitude for not more than seven years, or to imprisonment for any term not more than two years with or without hard labour. The abduction or unlawfully taking away an unmarried girl under sixteen out of the possession and against the will of her father or mother, or any other person having the lawful care or charge of her, is a misdemeanour under the same act. The term is used in much the same sense in the United States.
The kidnapping or forcible taking away of persons to serve at sea is treated underImpressment.
The kidnapping or forcible taking away of persons to serve at sea is treated underImpressment.
KIDNEY DISEASES.1(For the anatomy of the kidneys, seeUrinary System.) The results of morbid processes in the kidney may be grouped under three heads: the actual lesions produced, the effects of these on the composition of the urine,and the effects of the kidney-lesion on the body at large. Affections of the kidney are congenital or acquired. When acquired they may be the result of a pathological process limited to the kidney, in which case they are spoken of as primary, or an accompaniment of disease in other parts of the body, when they may be spoken of as secondary.
Congenital Affections.—The principal congenital affections are anomalies in the number or position of the kidneys or of their ducts; atrophy; cystic disease and growths. The most common abnormality is the existence of asingle kidney; rarely a supernumerary kidney may be present. The presence of a single kidney may be due to failure of development, or to atrophy in foetal life; it may also be dependent on the fusion of originally separate kidneys in such a way as to lead to the formation of ahorse-shoe kidney, the two organs being connected at their lower ends. In some cases of horse-shoe kidney the organs are united merely by fibrous tissue. Occasionally the two kidneys are fused end to end, with two ureters. A third variety is that where the fusion is more complete, producing a disk-like mass with two ureters. The kidneys may be situated inabnormal positions; thus they may be in front of the sacro-iliac articulation, in the pelvis, or in the iliac fossa. The importance of such displacements lies in the fact that the organs may be mistaken for tumours. In some casesatrophyis associated with mal-development, so that only the medullary portion of the kidney is developed; in others it is associated with arterial obstruction, and sometimes it may be dependent upon obstruction of the ureter. Incongenital cystic diseasethe organ is transformed into a mass of cysts, and the enlargement of the kidneys may be so great as to produce difficulties in birth. The cystic degeneration is caused by obstruction of the uriniferous tubules or by anomalies in development, with persistence of portions of the Wolffian body. In some cases cystic degeneration is accompanied by anomalies in the ureters and in the arterial supply.Growths of the kidneyare sometimes found in infants; they are usually malignant, and may consist of a peculiar form of sarcoma, which has been spoken of as rhabdo-sarcoma, owing to the presence in the mass of involuntary muscular fibres. The existence of these tumours is dependent on anomalies of development; the tissue which forms the primitive kidney belongs to the same layer as that which gives rise to the muscular system (mesoblast).Anomalies of the excretory ducts: in some cases the ureter is double, in others it is greatly dilated; in others the pelvis of the kidney may be greatly dilated, with or without dilatation of the ureter.Acquired Affections. Movable Kidney.—One or both of the kidneys in the adult may be preternaturally mobile. This condition is more common in women, and is usually the result of a severe shaking or other form of injury, or of the abdominal walls becoming lax as a sequel to abdominal distension, to emaciation or pregnancy, or to the effects of tight-lacing. The more extreme forms of movable kidney are dependent, generally, on anomalies in the arrangement of the peritoneum, so that the organ has a partial mesentery; and to this condition, where the kidney can be moved freely from one part of the abdomen to another, the termfloating kidneyis applied. But more usually the organ is loose under the peritoneum, and not efficiently supported in its fatty bed. Movable kidney produces a variety of symptoms, such as pain in the loin and back, faintness, nausea and vomiting—and the function of the organ may be seriously interfered with, owing to the ureter becoming kinked. In this way hydronephrosis, or distension of the kidney with urine, may be produced. The return of blood through the renal vein may also be hindered, and temporary vascular engorgement of the kidney, with haematuria, may be produced.In some cases the movable kidney may be satisfactorily kept in its place by a pad and belt, but in other cases an operation has to be undertaken. This consists in exposing the kidney (generally the right) through an incision below the last rib, and fixing it in its proper position by several permanent sutures of silk or silkworm gut. The operation is neither difficult nor dangerous, and its results are excellent.Embolism.—The arrangement of the blood-vessels of the kidney is peculiarly favourable to the production of wedge-shaped areas of necrosis, the result of a blocking by clots. Sometimes the clot is detached from the interior of the heart, the effect being an arrest of the circulation in the part of the kidney supplied by the blocked artery. In other cases, the plug is infective owing to the presence of septic micro-organisms, and this is likely to lead to the formation of small pyaemic abscesses. It is exceptional for the large branches of the renal artery to be blocked, so that the symptoms produced in the ordinary cases are only the temporary appearance of blood or albumen in the urine. Blocking of the main renal vessels as a result of disease of the walls of the vessels may lead to disorganization of the kidneys. Blocking of the veins, leading to extreme congestion of the kidney, also occurs. It is seen in cases of extreme weakness and wasting, sometimes in septic conditions, as in puerperal pyaemia, where a clot, formed first in one of the pelvic veins, may spread up the vena cava and secondarily block the renal veins. Thrombosis of the renal vein also occurs in malignant disease of the kidney and in certain forms of chronic Bright’s disease.Passive congestionof the kidneys occurs in heart-diseases and lung-diseases, where the return of venous blood is interfered with. It may also be produced by tumours pressing on the vena cava. The engorged kidneys become brownish red, enlarged and fibroid, and they secrete a scanty, high-coloured urine.Active congestionis produced by the excretion in the urine of such materials as turpentine and cantharides and the toxins of various diseases. These irritants produce engorgement and inflammation of the kidney, much as they would that of any other structures with which they come in contact. Renal disturbance is often the result of the excretion of microbic poisons. Extreme congestion of the kidneys may be produced by exposure to cold, owing to some intimate relationship existing between the cutaneous and the renal vessels, the constriction of the one being accompanied by the dilatation of the other. Infective diseases, such as typhoid fever, pneumonia, scarlet fever, in fact, most acute specific diseases, produce during their height a temporary nephritis, not usually followed by permanent alteration in the kidney; but some acute diseases cause a nephritis which may lay the foundation of permanent renal disease. This is most common as a result of scarlet fever.Bright’s diseaseis the term applied to certain varieties of acute and chronic inflammation of the kidney. Three forms are usually recognized—acute, chronic and the granular or cirrhotic kidney. In the more common form of granular kidney the renal lesion is only part of a widespread affection involving the whole arterial system, and is not actually related to Bright’s disease.Chronic Bright’s diseaseis sometimes the sequel to acute Bright’s disease, but in a great number of cases the malady is chronic from the beginning. The lesions of the kidney are probably produced by irritation of the kidney-structures owing to the excretion of toxic substances either ingested or formed in the body; it is thought by some that the malady may arise as a result of exposure to cold. The principal causes of Bright’s disease are alcoholism, gout, pregnancy and the action of such poisons as lead; it may also occur as a sequel to acute diseases, such as scarlet fever. Persons following certain occupations are peculiarly liable to Bright’s disease,e.g.engineers who work in hot shops and pass out into the cold air scantily clothed; and painters, in whom the malady is dependent on the action of lead on the kidney. In the case of alcohol and lead the poison is ingested; in the case of scarlet fever, pneumonia, and perhaps pregnancy, the toxic agent causing the renal affection is formed in the body. In Bright’s disease all the elements of the kidney, the glomeruli, the tubular epithelium, and the interstitial tissue, are affected. When the disease follows scarlet fever, the glomerular structures are mostly affected, the capsules being thickened by fibrous tissue, and the glomerular tuft compressed and atrophied. The epithelium of the convoluted tubules undergoes degeneration; considerable quantities of it are shed, and form the well-known casts in the urine. The tubules become blocked by the epithelium, and distended with the pent-up urine; this is one cause of the increase in size that the kidneys undergo in certain forms of Bright’s disease. The lesions in the tubules and in the glomeruli are not generally uniform. The interstitial tissue is always affected, and exudation, proliferation and formation of fibrous tissue occur. In the granular and contracted kidney the lesion in the interstitial tissue reaches a high degree of development, little renal secreting tissue being left. Such tubules as remain are dilated, and the epithelium lining them is altered, the cells becoming hyaline and losing their structure. The vessels are narrowed owing to thickening of the subendothelial layer, and the muscular coat undergoes hypertrophic and fibroid changes, so that the vessels are abnormally rigid. When the overgrowth of fibrous tissue is considerable, the surface of the organ becomes uneven, and it is for this reason that the termgranular kidneyhas been applied to the condition. In acute Bright’s disease the kidney is increased in size and engorged with blood, the changes described above being in active progress. In the chronic form the kidney may be large or small, and is usually white or mottled. If large, the cortex is thickened, pale and waxy, and the pyramids are congested; if small, the fibrous change has advanced and the cortex is diminished. Bright’s disease, both acute and chronic, is essentially a disease of the cortical secreting portion of the kidney. The true granular kidney, classified by some as a third variety, is usually part of a general arterial degeneration, the overgrowth of fibrous tissue in the kidney and the lesions in the arteries being well marked.The principal degenerations affecting the kidney are the fatty and the albuminoid.Fatty degenerationoften reaches a high degree in alcoholics, where fatty degeneration of the heart and liver are also present.Albuminoid diseaseis frequently associated with some varieties of Bright’s disease, and is also seen as a result of chronic bone disease, or of long-continued suppuration involving other parts of the body, or of syphilis. It is due to irritation of the kidneys by toxic products.Growths of the Kidney.—The principal growths are tubercle, adenoma, sarcoma and carcinoma. In addition, fatty and fibrous growths, the nodules of glanders and the gummata of syphilis, may be mentioned. Tuberculous disease is sometimes primary; more frequently it is secondary to tubercle in other portions of the genito-urinary apparatus. The genito-urinary tract may be infected bytubercle in two ways;ascending, in which the primary lesion is in the testicle, epididymis, or urinary bladder, the lesion travelling up by the ureter or the lymphatics to the kidney;descending, where the tubercle bacillus reaches the kidney through the blood-vessels. In the latter case, miliary tubercles, as scattered granules, are seen, especially in the cortex of the kidney; the lesion is likely to be bilateral. In primary tuberculosis, and in ascending tuberculosis, the lesion is at first unilateral.Malignant diseaseof the kidney takes the form of sarcoma or carcinoma. Sometimes it is dependent on the malignant growths starting in what are spoken of as “adrenal rests” in the cortex of the kidney. Sarcoma is most often seen in the young; carcinoma in the middle-aged and elderly. Carcinoma may be primary or secondary, but the kidney is not so prone to malignant disease as other organs, such as the stomach, bowel or liver.Cystic Kidneys.—Cysts may be single—sometimes of large size. Scattered small cysts are met with in chronic Bright’s disease and in granular contracted kidney, where the dilatation of tubules reaches a high degree. Certain growths, such as adenomata, are liable to cystic degeneration, and cysts are also found in malignant disease. Finally, there is a rare condition of general cystic disease somewhat similar to the congenital affection. In this form the kidneys, greatly enlarged, consist of a congeries of cysts separated by the remains of renal tissue.Parasitic Affections.—The more common parasites affecting the kidney, or some other portion of the urinary tract, and causing disease, are filaria, bilharzia and the cysticercus form of thetaenia echinococcus(hydatids). The presence offilariain the thoracic duct and other lymph-channels may determine the presence of chyle in the urine, together with the ova and young forms of the filaria, owing to the distension and rupture of a lymphatic vessel into some portion of the urinary tract. This is the common cause of chyluria in hot climates, but chyluria is occasionally seen in the United Kingdom without filaria.Bilharzia, especially in Egypt and South Africa, causes haematuria. The cysticercus form of thetaenia echinococcusleads to the production of hydatid cysts in the kidney; this organ, however, is not so often affected as the liver.Stone in the Kidney.—Calculi are frequently found in the kidney, consisting usually of uric acid, sometimes of oxalates, more rarely of phosphates. Calculous disease of the bladder (q.v.) is generally the sequel to the formation of a stone in the kidney, which, passing down, becomes coated by the salts in the urine. Calculi are usually formed in the pelvis of the kidney, and their formation is dependent either on the excessive amounts of uric acid, oxalic acid, &c., in the urine, or on an alteration in the composition of the urine, such as increased acidity, or on uric acid or oxalate of lime being present in an abnormal amount. The formation of abnormal crystals is often due to the presence of some colloid, such as blood, mucus or albumen, in the secretion, modifying the crystalline form. Once a minute calculus has been formed, its subsequent growth is highly probable, owing to the deposition on it of the urinary constituent forming it. Calculi formed in the pelvis of the kidney may be single and may reach a very large size, forming, indeed, an actual cast of the interior of the expanded kidney. At other times they are multiple and of varying size. They may give rise to no symptoms, or on the other hand may cause distressing renal colic, especially when they are small and loose and are passed or are trying to be passed. Serious complications may result from the presence of a stone in the kidney, such as hydronephrosis, from the urinary secretion being pent up behind the obstruction, or complete suppression, which is apparently produced reflexly through the nervous system. In such cases the surgical removal of the stone is often followed by the restoration of the renal secretion.The symptoms ofrenal calculusmay be very slight, or they may be entirely absent if the stone is moulding itself into the interior of the kidney; but if the stone is movable, heavy and rough, it may cause great distress, especially during exercise. There will probably be blood in the urine; and there will be pain in the loin and thigh and down into the testicle. The testicle also may be drawn up by its suspensory muscle, and there may be irritability of the bladder. With stone in one kidney the pains may be actually referred to the kidney of the other side. Generally, but not always, there is tenderness in the loin. If the stone is composed of lime it may throw a shadow on the Röntgen plate, but other stones may give no shadow.Renal colicis the acute pain felt when a small stone is travelling down the ureter to the bladder. The pain is at times so acute that fomentations, morphia and hot baths fail to ease it, and nothing short of chloroform gives relief.For theoperative treatment of renal calculusan incision is made a little below the last rib, and, the muscles having been traversed, the kidney is reached on the surface which is not covered by peritoneum. Most likely the stone is then felt, so it is cut down upon and removed. If it is not discoverable on gently pinching the kidney between the finger and thumb, the kidney had better be opened in its convex border and explored by the finger. Often it has happened that when a man has presented most of the symptoms of renal calculus and has been operated on with a negative result as regards finding a stone, all the symptoms have nevertheless disappeared as the direct result of the blank operation.Pyelitis.—Inflammation of the pelvis of the kidney is generally produced by the extension of gonorrhoeal or other septic inflammation upwards from the bladder and lower urinary tract, or by the presence of stone or of tubercle in the pelvis of the kidney. Pyonephrosis, or distension of the kidney with pus, may result as a sequel to pyelitis or as a complication of hydronephrosis; in many cases the inflammation spreads to the capsule of the kidney, and leads to the formation of an abscess outside the kidney—aperinephritic abscess. In some cases a perinephritic abscess results from a septic plug in a blood-vessel of the kidney, or it may occur as the result of an injury to the loose cellular tissue surrounding the kidney, without lesion of the kidney.Hydronephrosis, or distension of the kidney with pent-up urine, results from obstruction of the ureter, although all obstructions of the ureter are not followed by it, calculous obstruction, as already noted, often causing complete suppression of urine. Obstruction of the ureter, causing hydronephrosis, is likely to be due to the impaction of a stone, or to pressure on the ureter from a tumour in the pelvis—as, for instance, a cancer of the uterus—or to some abnormality of the ureter. Sometimes a kink of the ureter of a movable kidney causes hydronephrosis. The hydronephrosis produced by obstruction of the ureter may be intermittent; and when a certain degree of distension is produced, either as a result of the shifting of the calculus or of some other cause, the obstruction is temporarily relieved in a great outflow of urine, and the urinary discharge is re-established. When the hydronephrosis has long existed the kidney is converted into a sac, the remains of the renal tissues being spread out as a thin layer.Effects on the Urine.—Diseases of the kidney produce alterations in the composition of the urine; either the proportion of the normal constituents being altered, or substances not normally present being excreted. In most diseases the quantity of urinary water is diminished, especially in those in which the activity of the circulation is impaired. There are diseases, however, more especially the granular kidney and certain forms of chronic Bright’s disease, in which the quantity of urinary water is considerably increased, notwithstanding the profound anatomical changes that have occurred in the kidney. There are two forms of suppression of the urine: one isobstructive suppression, seen where the ureter is blocked by stone or other morbid process; the other isnon-obstructive suppression, which is apt to occur in advanced diseases of the kidney. In other cases complete suppression may occur as the result of injuries to distant parts of the body, as after severe surgical operations. In some diseases in which the quantity of urinary water excreted is normal, or even greater than normal, the efficiency of the renal activity is really diminished, inasmuch as the urine contains few solids. In estimating the efficiency of the kidneys, it is necessary to take into consideration the so-called “solid urine,” that is to say, the quantity of solid matter daily excreted, as shown by the specific gravity of the urine. The nitrogenous constituents—urea, uric acid, creatinin, &c.—vary greatly in amount in different diseases. In most renal diseases the quantities of these substances are diminished because of the physiological impairment of the kidney. The chief abnormal constituents of the urine are serum-albumen, serum-globulin, albumoses (albuminuria), blood (haematuria), blood pigment (haemoglobinuria), pus (pyuria), chyle (chyluria) and pigments such as melanuria and urobilinuria.Effects on the Body at large.—These may be divided into the persistent and the intermittent or transitory. The most important persistent effects produced by disease of the kidney are, first, nutritional changes leading to general ill health, wasting and cachexia; and, secondly, certain cardio-vascular phenomena, such as enlargement (hypertrophy) of the heart, and thickening of the inner, and degeneration of the middle, coat of the smaller arteries. Amongst the intermittent or transitory effects are dropsy, secondary inflammations of certain organs and serous cavities, and uraemia. Some of these effects are seen in every form of severe kidney disease, and uraemia may occur in any advanced kidney disease. Renal dropsy is chiefly seen in certain forms of Bright’s disease, and the cardiac and arterial changes are commonest in cases of granular or contracted kidney, but may be absent in other diseases which destroy the kidney tissue, such as hydronephrosis.Uraemiais a toxic condition, and three varieties of it are recognized—the acute, the chronic and the latent. Many of these effects are dependent upon the action of poisons retained in the body owing to the deficient action of the kidneys. It is also probable that abnormal substances having a toxic action are produced as a result of a perverted metabolism. Uraemia is of toxic origin, and it is probable that the dropsy of renal disease is due to effects produced in the capillaries by the presence of abnormal substances in the blood. High arterial tension, cardiac hypertrophy and arterial degeneration may also be of toxic origin, or they may be produced by an attempt of the body to maintain an active circulation through the greatly diminished amount of kidney tissue available.Rupture of the kidneymay result from a kick or other direct injury. Vomiting and collapse are likely to ensue, and most likely blood will appear in the urine, or a tumour composed of blood and urine may form in the renal region. An incision made into the swelling from the loin may enable the surgeon to see the torn kidney. An attempt should be made to save the kidney by suturing and draining; unlessthe damage is obviously past repair, the kidney should not be removed without giving nature a chance.
Congenital Affections.—The principal congenital affections are anomalies in the number or position of the kidneys or of their ducts; atrophy; cystic disease and growths. The most common abnormality is the existence of asingle kidney; rarely a supernumerary kidney may be present. The presence of a single kidney may be due to failure of development, or to atrophy in foetal life; it may also be dependent on the fusion of originally separate kidneys in such a way as to lead to the formation of ahorse-shoe kidney, the two organs being connected at their lower ends. In some cases of horse-shoe kidney the organs are united merely by fibrous tissue. Occasionally the two kidneys are fused end to end, with two ureters. A third variety is that where the fusion is more complete, producing a disk-like mass with two ureters. The kidneys may be situated inabnormal positions; thus they may be in front of the sacro-iliac articulation, in the pelvis, or in the iliac fossa. The importance of such displacements lies in the fact that the organs may be mistaken for tumours. In some casesatrophyis associated with mal-development, so that only the medullary portion of the kidney is developed; in others it is associated with arterial obstruction, and sometimes it may be dependent upon obstruction of the ureter. Incongenital cystic diseasethe organ is transformed into a mass of cysts, and the enlargement of the kidneys may be so great as to produce difficulties in birth. The cystic degeneration is caused by obstruction of the uriniferous tubules or by anomalies in development, with persistence of portions of the Wolffian body. In some cases cystic degeneration is accompanied by anomalies in the ureters and in the arterial supply.Growths of the kidneyare sometimes found in infants; they are usually malignant, and may consist of a peculiar form of sarcoma, which has been spoken of as rhabdo-sarcoma, owing to the presence in the mass of involuntary muscular fibres. The existence of these tumours is dependent on anomalies of development; the tissue which forms the primitive kidney belongs to the same layer as that which gives rise to the muscular system (mesoblast).Anomalies of the excretory ducts: in some cases the ureter is double, in others it is greatly dilated; in others the pelvis of the kidney may be greatly dilated, with or without dilatation of the ureter.
Acquired Affections. Movable Kidney.—One or both of the kidneys in the adult may be preternaturally mobile. This condition is more common in women, and is usually the result of a severe shaking or other form of injury, or of the abdominal walls becoming lax as a sequel to abdominal distension, to emaciation or pregnancy, or to the effects of tight-lacing. The more extreme forms of movable kidney are dependent, generally, on anomalies in the arrangement of the peritoneum, so that the organ has a partial mesentery; and to this condition, where the kidney can be moved freely from one part of the abdomen to another, the termfloating kidneyis applied. But more usually the organ is loose under the peritoneum, and not efficiently supported in its fatty bed. Movable kidney produces a variety of symptoms, such as pain in the loin and back, faintness, nausea and vomiting—and the function of the organ may be seriously interfered with, owing to the ureter becoming kinked. In this way hydronephrosis, or distension of the kidney with urine, may be produced. The return of blood through the renal vein may also be hindered, and temporary vascular engorgement of the kidney, with haematuria, may be produced.
In some cases the movable kidney may be satisfactorily kept in its place by a pad and belt, but in other cases an operation has to be undertaken. This consists in exposing the kidney (generally the right) through an incision below the last rib, and fixing it in its proper position by several permanent sutures of silk or silkworm gut. The operation is neither difficult nor dangerous, and its results are excellent.
Embolism.—The arrangement of the blood-vessels of the kidney is peculiarly favourable to the production of wedge-shaped areas of necrosis, the result of a blocking by clots. Sometimes the clot is detached from the interior of the heart, the effect being an arrest of the circulation in the part of the kidney supplied by the blocked artery. In other cases, the plug is infective owing to the presence of septic micro-organisms, and this is likely to lead to the formation of small pyaemic abscesses. It is exceptional for the large branches of the renal artery to be blocked, so that the symptoms produced in the ordinary cases are only the temporary appearance of blood or albumen in the urine. Blocking of the main renal vessels as a result of disease of the walls of the vessels may lead to disorganization of the kidneys. Blocking of the veins, leading to extreme congestion of the kidney, also occurs. It is seen in cases of extreme weakness and wasting, sometimes in septic conditions, as in puerperal pyaemia, where a clot, formed first in one of the pelvic veins, may spread up the vena cava and secondarily block the renal veins. Thrombosis of the renal vein also occurs in malignant disease of the kidney and in certain forms of chronic Bright’s disease.
Passive congestionof the kidneys occurs in heart-diseases and lung-diseases, where the return of venous blood is interfered with. It may also be produced by tumours pressing on the vena cava. The engorged kidneys become brownish red, enlarged and fibroid, and they secrete a scanty, high-coloured urine.
Active congestionis produced by the excretion in the urine of such materials as turpentine and cantharides and the toxins of various diseases. These irritants produce engorgement and inflammation of the kidney, much as they would that of any other structures with which they come in contact. Renal disturbance is often the result of the excretion of microbic poisons. Extreme congestion of the kidneys may be produced by exposure to cold, owing to some intimate relationship existing between the cutaneous and the renal vessels, the constriction of the one being accompanied by the dilatation of the other. Infective diseases, such as typhoid fever, pneumonia, scarlet fever, in fact, most acute specific diseases, produce during their height a temporary nephritis, not usually followed by permanent alteration in the kidney; but some acute diseases cause a nephritis which may lay the foundation of permanent renal disease. This is most common as a result of scarlet fever.
Bright’s diseaseis the term applied to certain varieties of acute and chronic inflammation of the kidney. Three forms are usually recognized—acute, chronic and the granular or cirrhotic kidney. In the more common form of granular kidney the renal lesion is only part of a widespread affection involving the whole arterial system, and is not actually related to Bright’s disease.Chronic Bright’s diseaseis sometimes the sequel to acute Bright’s disease, but in a great number of cases the malady is chronic from the beginning. The lesions of the kidney are probably produced by irritation of the kidney-structures owing to the excretion of toxic substances either ingested or formed in the body; it is thought by some that the malady may arise as a result of exposure to cold. The principal causes of Bright’s disease are alcoholism, gout, pregnancy and the action of such poisons as lead; it may also occur as a sequel to acute diseases, such as scarlet fever. Persons following certain occupations are peculiarly liable to Bright’s disease,e.g.engineers who work in hot shops and pass out into the cold air scantily clothed; and painters, in whom the malady is dependent on the action of lead on the kidney. In the case of alcohol and lead the poison is ingested; in the case of scarlet fever, pneumonia, and perhaps pregnancy, the toxic agent causing the renal affection is formed in the body. In Bright’s disease all the elements of the kidney, the glomeruli, the tubular epithelium, and the interstitial tissue, are affected. When the disease follows scarlet fever, the glomerular structures are mostly affected, the capsules being thickened by fibrous tissue, and the glomerular tuft compressed and atrophied. The epithelium of the convoluted tubules undergoes degeneration; considerable quantities of it are shed, and form the well-known casts in the urine. The tubules become blocked by the epithelium, and distended with the pent-up urine; this is one cause of the increase in size that the kidneys undergo in certain forms of Bright’s disease. The lesions in the tubules and in the glomeruli are not generally uniform. The interstitial tissue is always affected, and exudation, proliferation and formation of fibrous tissue occur. In the granular and contracted kidney the lesion in the interstitial tissue reaches a high degree of development, little renal secreting tissue being left. Such tubules as remain are dilated, and the epithelium lining them is altered, the cells becoming hyaline and losing their structure. The vessels are narrowed owing to thickening of the subendothelial layer, and the muscular coat undergoes hypertrophic and fibroid changes, so that the vessels are abnormally rigid. When the overgrowth of fibrous tissue is considerable, the surface of the organ becomes uneven, and it is for this reason that the termgranular kidneyhas been applied to the condition. In acute Bright’s disease the kidney is increased in size and engorged with blood, the changes described above being in active progress. In the chronic form the kidney may be large or small, and is usually white or mottled. If large, the cortex is thickened, pale and waxy, and the pyramids are congested; if small, the fibrous change has advanced and the cortex is diminished. Bright’s disease, both acute and chronic, is essentially a disease of the cortical secreting portion of the kidney. The true granular kidney, classified by some as a third variety, is usually part of a general arterial degeneration, the overgrowth of fibrous tissue in the kidney and the lesions in the arteries being well marked.
The principal degenerations affecting the kidney are the fatty and the albuminoid.Fatty degenerationoften reaches a high degree in alcoholics, where fatty degeneration of the heart and liver are also present.Albuminoid diseaseis frequently associated with some varieties of Bright’s disease, and is also seen as a result of chronic bone disease, or of long-continued suppuration involving other parts of the body, or of syphilis. It is due to irritation of the kidneys by toxic products.
Growths of the Kidney.—The principal growths are tubercle, adenoma, sarcoma and carcinoma. In addition, fatty and fibrous growths, the nodules of glanders and the gummata of syphilis, may be mentioned. Tuberculous disease is sometimes primary; more frequently it is secondary to tubercle in other portions of the genito-urinary apparatus. The genito-urinary tract may be infected bytubercle in two ways;ascending, in which the primary lesion is in the testicle, epididymis, or urinary bladder, the lesion travelling up by the ureter or the lymphatics to the kidney;descending, where the tubercle bacillus reaches the kidney through the blood-vessels. In the latter case, miliary tubercles, as scattered granules, are seen, especially in the cortex of the kidney; the lesion is likely to be bilateral. In primary tuberculosis, and in ascending tuberculosis, the lesion is at first unilateral.Malignant diseaseof the kidney takes the form of sarcoma or carcinoma. Sometimes it is dependent on the malignant growths starting in what are spoken of as “adrenal rests” in the cortex of the kidney. Sarcoma is most often seen in the young; carcinoma in the middle-aged and elderly. Carcinoma may be primary or secondary, but the kidney is not so prone to malignant disease as other organs, such as the stomach, bowel or liver.
Cystic Kidneys.—Cysts may be single—sometimes of large size. Scattered small cysts are met with in chronic Bright’s disease and in granular contracted kidney, where the dilatation of tubules reaches a high degree. Certain growths, such as adenomata, are liable to cystic degeneration, and cysts are also found in malignant disease. Finally, there is a rare condition of general cystic disease somewhat similar to the congenital affection. In this form the kidneys, greatly enlarged, consist of a congeries of cysts separated by the remains of renal tissue.
Parasitic Affections.—The more common parasites affecting the kidney, or some other portion of the urinary tract, and causing disease, are filaria, bilharzia and the cysticercus form of thetaenia echinococcus(hydatids). The presence offilariain the thoracic duct and other lymph-channels may determine the presence of chyle in the urine, together with the ova and young forms of the filaria, owing to the distension and rupture of a lymphatic vessel into some portion of the urinary tract. This is the common cause of chyluria in hot climates, but chyluria is occasionally seen in the United Kingdom without filaria.Bilharzia, especially in Egypt and South Africa, causes haematuria. The cysticercus form of thetaenia echinococcusleads to the production of hydatid cysts in the kidney; this organ, however, is not so often affected as the liver.
Stone in the Kidney.—Calculi are frequently found in the kidney, consisting usually of uric acid, sometimes of oxalates, more rarely of phosphates. Calculous disease of the bladder (q.v.) is generally the sequel to the formation of a stone in the kidney, which, passing down, becomes coated by the salts in the urine. Calculi are usually formed in the pelvis of the kidney, and their formation is dependent either on the excessive amounts of uric acid, oxalic acid, &c., in the urine, or on an alteration in the composition of the urine, such as increased acidity, or on uric acid or oxalate of lime being present in an abnormal amount. The formation of abnormal crystals is often due to the presence of some colloid, such as blood, mucus or albumen, in the secretion, modifying the crystalline form. Once a minute calculus has been formed, its subsequent growth is highly probable, owing to the deposition on it of the urinary constituent forming it. Calculi formed in the pelvis of the kidney may be single and may reach a very large size, forming, indeed, an actual cast of the interior of the expanded kidney. At other times they are multiple and of varying size. They may give rise to no symptoms, or on the other hand may cause distressing renal colic, especially when they are small and loose and are passed or are trying to be passed. Serious complications may result from the presence of a stone in the kidney, such as hydronephrosis, from the urinary secretion being pent up behind the obstruction, or complete suppression, which is apparently produced reflexly through the nervous system. In such cases the surgical removal of the stone is often followed by the restoration of the renal secretion.
The symptoms ofrenal calculusmay be very slight, or they may be entirely absent if the stone is moulding itself into the interior of the kidney; but if the stone is movable, heavy and rough, it may cause great distress, especially during exercise. There will probably be blood in the urine; and there will be pain in the loin and thigh and down into the testicle. The testicle also may be drawn up by its suspensory muscle, and there may be irritability of the bladder. With stone in one kidney the pains may be actually referred to the kidney of the other side. Generally, but not always, there is tenderness in the loin. If the stone is composed of lime it may throw a shadow on the Röntgen plate, but other stones may give no shadow.
Renal colicis the acute pain felt when a small stone is travelling down the ureter to the bladder. The pain is at times so acute that fomentations, morphia and hot baths fail to ease it, and nothing short of chloroform gives relief.
For theoperative treatment of renal calculusan incision is made a little below the last rib, and, the muscles having been traversed, the kidney is reached on the surface which is not covered by peritoneum. Most likely the stone is then felt, so it is cut down upon and removed. If it is not discoverable on gently pinching the kidney between the finger and thumb, the kidney had better be opened in its convex border and explored by the finger. Often it has happened that when a man has presented most of the symptoms of renal calculus and has been operated on with a negative result as regards finding a stone, all the symptoms have nevertheless disappeared as the direct result of the blank operation.
Pyelitis.—Inflammation of the pelvis of the kidney is generally produced by the extension of gonorrhoeal or other septic inflammation upwards from the bladder and lower urinary tract, or by the presence of stone or of tubercle in the pelvis of the kidney. Pyonephrosis, or distension of the kidney with pus, may result as a sequel to pyelitis or as a complication of hydronephrosis; in many cases the inflammation spreads to the capsule of the kidney, and leads to the formation of an abscess outside the kidney—aperinephritic abscess. In some cases a perinephritic abscess results from a septic plug in a blood-vessel of the kidney, or it may occur as the result of an injury to the loose cellular tissue surrounding the kidney, without lesion of the kidney.
Hydronephrosis, or distension of the kidney with pent-up urine, results from obstruction of the ureter, although all obstructions of the ureter are not followed by it, calculous obstruction, as already noted, often causing complete suppression of urine. Obstruction of the ureter, causing hydronephrosis, is likely to be due to the impaction of a stone, or to pressure on the ureter from a tumour in the pelvis—as, for instance, a cancer of the uterus—or to some abnormality of the ureter. Sometimes a kink of the ureter of a movable kidney causes hydronephrosis. The hydronephrosis produced by obstruction of the ureter may be intermittent; and when a certain degree of distension is produced, either as a result of the shifting of the calculus or of some other cause, the obstruction is temporarily relieved in a great outflow of urine, and the urinary discharge is re-established. When the hydronephrosis has long existed the kidney is converted into a sac, the remains of the renal tissues being spread out as a thin layer.
Effects on the Urine.—Diseases of the kidney produce alterations in the composition of the urine; either the proportion of the normal constituents being altered, or substances not normally present being excreted. In most diseases the quantity of urinary water is diminished, especially in those in which the activity of the circulation is impaired. There are diseases, however, more especially the granular kidney and certain forms of chronic Bright’s disease, in which the quantity of urinary water is considerably increased, notwithstanding the profound anatomical changes that have occurred in the kidney. There are two forms of suppression of the urine: one isobstructive suppression, seen where the ureter is blocked by stone or other morbid process; the other isnon-obstructive suppression, which is apt to occur in advanced diseases of the kidney. In other cases complete suppression may occur as the result of injuries to distant parts of the body, as after severe surgical operations. In some diseases in which the quantity of urinary water excreted is normal, or even greater than normal, the efficiency of the renal activity is really diminished, inasmuch as the urine contains few solids. In estimating the efficiency of the kidneys, it is necessary to take into consideration the so-called “solid urine,” that is to say, the quantity of solid matter daily excreted, as shown by the specific gravity of the urine. The nitrogenous constituents—urea, uric acid, creatinin, &c.—vary greatly in amount in different diseases. In most renal diseases the quantities of these substances are diminished because of the physiological impairment of the kidney. The chief abnormal constituents of the urine are serum-albumen, serum-globulin, albumoses (albuminuria), blood (haematuria), blood pigment (haemoglobinuria), pus (pyuria), chyle (chyluria) and pigments such as melanuria and urobilinuria.
Effects on the Body at large.—These may be divided into the persistent and the intermittent or transitory. The most important persistent effects produced by disease of the kidney are, first, nutritional changes leading to general ill health, wasting and cachexia; and, secondly, certain cardio-vascular phenomena, such as enlargement (hypertrophy) of the heart, and thickening of the inner, and degeneration of the middle, coat of the smaller arteries. Amongst the intermittent or transitory effects are dropsy, secondary inflammations of certain organs and serous cavities, and uraemia. Some of these effects are seen in every form of severe kidney disease, and uraemia may occur in any advanced kidney disease. Renal dropsy is chiefly seen in certain forms of Bright’s disease, and the cardiac and arterial changes are commonest in cases of granular or contracted kidney, but may be absent in other diseases which destroy the kidney tissue, such as hydronephrosis.Uraemiais a toxic condition, and three varieties of it are recognized—the acute, the chronic and the latent. Many of these effects are dependent upon the action of poisons retained in the body owing to the deficient action of the kidneys. It is also probable that abnormal substances having a toxic action are produced as a result of a perverted metabolism. Uraemia is of toxic origin, and it is probable that the dropsy of renal disease is due to effects produced in the capillaries by the presence of abnormal substances in the blood. High arterial tension, cardiac hypertrophy and arterial degeneration may also be of toxic origin, or they may be produced by an attempt of the body to maintain an active circulation through the greatly diminished amount of kidney tissue available.
Rupture of the kidneymay result from a kick or other direct injury. Vomiting and collapse are likely to ensue, and most likely blood will appear in the urine, or a tumour composed of blood and urine may form in the renal region. An incision made into the swelling from the loin may enable the surgeon to see the torn kidney. An attempt should be made to save the kidney by suturing and draining; unlessthe damage is obviously past repair, the kidney should not be removed without giving nature a chance.