1. Secondary to infection in some site of the body; commonest cause
is haemolytic streptococcal infection of the respiratory tract, other
organisms may be pneumococcus, or Streptococcus viridans.
1. Retrogressive changes in tubular epithelium, affecting particularly
that of proximal convoluted tubules.
2. Desquamative nephritis. Excessive desquamation of the degenerated
and necrotic epithelium.
Glomerular lesions may of three types.
A. Acute degenerative glomerulitis
1. Blood in the subcapsular space and adjacent tubules; resulting from
deterioration of the cells of capillary loops.
B. Acute exudative glomerulitis
C. Acute proliferative glomerulitis
Most common type may be of two forms:
1. Intracapillary form: The entire tuft is considerably enlarged and occupies the entire capsular space. The capillary loose are free of blood, due to swelling and proliferation of the capillary endothelium. Occasionally, a few polymorphs may be observed in the capillary loops and interstitial connective tissue.
2. Extracapillary or subcapsular form: Swelling or proliferation of the epithelium underlying the capsule of Bowman. The mass of cells may form a circular rim around the glomeruli or a crescentic mass.
1. Enlarged, slightly or considerably
1. Marked swelling and pallor of the cortex
1. Glomeruli enlarged 3-4 times; without blood.
5. Cloudy swelling, fatty degeneration, or necrosis in convoluted tubules.
6. Collections of small round cells in the interstital tissue.
1. Size initially normal; later shrunken with granular surface.
1. Renal archetecture completely lost.
Modes of Infection
1. Ascent from below in:
1. Diabetes mellitus
The lesions may be local or diffuse. The changes vary with the stage of the disease.
A. In acute stage
B. In chronic cases
1. Small abscesses with widespread interstitial infiltration of streaky linear round cells and polymorphs.
2. Renal tubules, destroyed and replaced by scar tissue.
3. Many tubules, especially in the scarred areas, are lined by flattened epithelium and filled with dense, acidophilic colloid like material.
4. Periglomerular fibrosis is marked even when the glomeruli are intact.
5. Round cell infiltration or fibrosis in the renal pelvis.
6. Arteries in the affected areas show endarterities obliterans.
Causes of Hydronephrosis
(b) In the bladder:
(c) In the urethra
1. Pelvis and calyces are greatly dilated.
Hydronephrotic fluid is relatively sterile as continuous circulation
is maintained by:
1. Initially only tubular atrophy; glomeruli normal.
Types of Nephrosclerosis
1. Benign hypertensive nephroscierosis
Benign Hypertensive Nephrosclerosis
On Cut Section
Malignant Hypertensive Nephrosclerosis
On Cut Section
1. Patches of interstitial change (cellular and fibrotic).
Causes of Contracted Granular Kidney
1. Benign hypertensive nephrosclerosis
Haemosiderosis and Haemoglobinuric Nephrosis
Syphilitic Lesions in the Kidney
1. Congenital interstitial nephritis
Congenital Interstitial Nephritis
The kidney of congenital syphilis is characterised by interstitial inflammation in association with great numbers of treponemas in the interstitial spaces, in the tubular lumen and among the tubular epithelial cells.
1. Manifests as sudden onset of nephrotic syndrome, without renal
Syphilitic Focal Interstitial Nephritis
Asymptomatic damage to the kidney in secondary stage of syphilis.
Structure of Renal Calculi
The calculus consists of a nucleus of organic matter around which urinary
salts are deposited in concentric layers which are bound together by a
colloid matrix of organic matter. The salts, although crystalline
in the urine, are in the form of amorphous granules in the calculus. The
calculi may consist of.
Mode of Formation
1. Infection. Infection is important in the secondary phosphate stone which is a common consequence of cystitis associated with enlargement of the prostate. It is probable that a mild infection is the starting point of all the uric acid and oxalate stones in the kidney, although, it is not readily detected like the gross infection which is responsible for the secondary phosphate stones. The type of the stone depends upon the reaction of the urine and that depends upon infection. A uric acid or oxalate stone is formed when the urine is acidic. Infection with pyogenic cocci turns the urine alkaline and the stone becomes coated with phosphate. Subsequent infection with Esch. coli may bring back an acidic reaction with deposition of uric acid or calcium oxalate.
2. Concentration of the crystalline salts. The relation of colloids of the urine to the crystalloids is probably of great importance. The presence of an abnormal colloid or absence of a normal one may cause crystalloids to be precipitated, especially if they are present in excess.
3. Parathyoid tumour. This is commonly associated with bilateral and recurring calculi. As a result of hyper-parathyroidism, calcium is removed from the bones, the blood is flooded with calcium and this tends to be deposited in the renal pelvis. Such stones have high content of calcium and phosphates.
4. Vitamin A deficiency. Lack of this vitamin leads to keratinization and desquamation of the epithelium of the renal pelvis which may form the nidus for a stone. It also affects the urinary colloids so that they fail to hold the crystalloids in solution.
5. Nephrocalcinosis. The term refers to the deposition of calcium and phosphorus in the renal tubules or in the interstitial tissue of the kidney. The condition is characterized by hypercalcinuria, negative calcium balance and evidence in skiagram. It is often associated with the formation of calculi.
6. Prolonged immobility. When patients such as paraplegics are confined to bed for long periods unable to move their limbs, the bones tend to become decalcified and phosphate stones are often formed.
The glomerular lesions of diabetic nephropathy are of three types:
The nodules are usually situated at the periphery of the affected
glomerulus. These are eosinophilic and show a laminated appearance when
stained with periodic acid Schiff reagent. The initial lesion probably
starts within the capillary wall. The hya
The diffuse glomerular lesion is more common than the nodular lesion and is the main cause of the reduced glomerular filtration rate and azotaemia characteristic of the later stages of diabetic glomerulosclerosis. The capillary walls are thickened by deposit of a substance rich in polysacharide. The basement membrane is probably first involved, with later extension to endothelial and epithelial cells. In the earlier stages, the changes are uneven within the same glomerulus and in different parts of the kidney. Later the whole glomerulus becomes hyalinised and bloodless and there is atrophy of the corresponding tubule. The diffuse lesion may occur without any evidence of nodular change but whenever there are nodular lesions, the diffuse change will be present in the other glomeruli.
The exudative lesion is the least common and least characteristic
abnormality of the glomerulus in diabetic nephropathy. It consists of an
eosinophilic structureless crescentic area surrounding the periphery of
a lobule of a glomerulus. It stains more
Other changes in diabetic nephropathy include usually severe renal vascular disease with hyaline change in the wall of arterioles and secondary areas of ischaemic atrophy. Pyelonephritis often occurs in diabetes mellitus especially in the later stages of diabetic nephropathy. Distal tubular or papillary necrosis is of frequent occurrence.
I. Pre-renal Causes:
1. Circulatory failure: (i) Cardiac (ii) Peripheral
2. Severe fluid and electrolyte imbalance
II. Renal Causes:
1. Acute glomerulonephritis
III. Post-renal Causes:
1. Obstruction in ureters
Uraemia is associated with headache, drowsiness, twitching of extremities, convulsions, coma and a group of other symptoms and signs. The features disclosed by biopsy are variable, but,there are renal lesions, degenerations of hypertrophic heart, cerebral edema, ulcerative ileocolitis and increased amount of urea in the renal cortex. Often bronchopneumonia is present as a terminal event.
2. Primary tubular disease:
3. Vascular disease:
Infections: (i) Chronic pyelonephritis (ii) Tuberculosis.
5. Metabolic renal diseases:
6. Congenital anomalies of the kidney:
7. Urinary tract obstruction:
It is a clinical syndrome characterised by:
The condition usually becomes apparent in early childhood and death
generally occurs before puberty. There is a widespread deposition of cystine
in different tissues (cystinosis), the cause of which is not known although
it implies a profound
A similar entity generally referred to as adult Fancony syndrome has been found as a familial condition in adults. It is not associated with cystine deposition and presents as a form of osteomalacia. Such biochemical abnormalities as the aminoaciduria and glycosuria may be recognized prior to development of any clinical symptoms.
The Nephrotic syndrome (or Lipid nephrosis is a clinical complex consisting of :-
(i) Proteinuria, principally albuminuria.
This clinical complex is referred to as pure nephrotic syndrome. It is distinguished from the impure, mixed or complicated nephrotic syndrome in which the following additional features are present:
(i) Haematuria (ii) Hypertension (iii) Pyuria (iv) Azotaemia.
2. Systemic disease:
3. Kidney disorders:
4. Chemical agents:
Vast majority of the cases of nephrotic syndrome are idiopathic. Only rarely the cause is known. The following theories have been forwarded to explain the etiology of idiopathic nephrotic syndrome :-
(i) A preceding streptococcal infection. In an established case of nephrosis,
subsequent recurrent streptococcal infections affect the disease process
Once the glomerular lesion, i.e., abnormality of the epithelial foot processes and subsequent basement membrane thickening, is established, oedema in nephrotic syndrome follows proteinuria. Albumin is the main protein lost though other protein fractions like alpha and gamma globulins also are lost considerably. Proteinuria is mainly responsible for hypoproteinaemia. Protein intake is also low because of accompanying anorexia and diminished absorption of ingested proteins, because of intestinal oedema. This may further add to hypoproteinemia.
Hypoproteinaemia leads to decreased colloidal osmotic pressure allowing escape of water into cellular tissue. This starts the oedema and sets up the factors which contribute further to accumulation of fluid in the body.
The escape of water from plasma leads to reduction of blood volume leading to hormonal disturbances concerned with water and electrolyte regulation. There is increased secretion of antidiuretic hormone (ADH) and aldosterone. Aldosterone retains sodium and alongwith that more and more water is retained. However, the retained water cannot be held in circulation because of hypoproteinaemia and is lost to the extracellular tissue causing further reduction in blood volume and the whole cycle repeats.
Like the interstitial tissue in all other organs, that of the kidney is also water-logged. This raises intrarenal hydrostatic pressure with its effect on venular patency. This raised internal venular resistance reduces the effective glomerular filtration and also increases tubular water absorption. The tense stretched capsule of the swollen kidney might be responsible for autonomic nerve stimulation causing afferent arteriolar spasm reducing glomerular filtration.
The cause of hyperchlolesterolaemia is not fully understood. It is believed that it results from increased synthesis of cholesterol and of lipoproteins, and can be induced by certain nephrotoxic sera.
2. Embryonal tumours
II. Renal Pelvis
Microscopic appearance. The tubules may be irregular or
dilated, papillary processes may project into them. Some of the cells are
small, dark or compact, but others may be large clear cells, so as to resemble
those of the clear cell carcinoma. The capsule, if at all present may be
penetrated by tumour cells.
Macroscopic appearance. The tumour arises in the upper or lower pole but more often in the middle portion of the kidney. It begins near capsule and enlarges to form a globular mass. Fibrous tissue may form a capsule around the tumour. The tumour is soft and in the cross-section is bulging, o yellow colour, bleeds freely and is often lobulated by fibrous trabeculae. There are numerous foci and masses of necrosis and haemorrhage; the tumour, often, compresses and distorts the pelvis and may invade it. Extension into the tributaries of the renal vein, into the main renal vein and even upto the vena cavae is not infrequent.
Microscopic appearance. It varies greatly. The most common form is made up of large cuboidal or polyhedral cells with clear vesicular cytoplasm which may contain fat or glycogen. The nuclei are small, fairly dense and often eccentric. These cells grow in bands and papillary projections from a delicate fibrous reticulum. containing many capillaries which may give an alveolated character to the tumour. Necrosis, haemorrhage and blood pigment are common, other tumours are made up of smaller cells with granular cytoplasm and dense, centrally disposed nuclei. In these tumours, the cells are usually in sheets and masses. In either form acini may be found and these are often papilliferous, However, there may be mixtures of these types of cells with preponderance of one or the other. The supporting connective tissue is richly vascularized.
Metastases are most frequent in lungs, liver, adrenals and bones and less frequent in kidney, spleen, heart and brain.
Wilm's tuniours (nephroblastoma). This is the commonest malignant
tumour of early childhood. It usually occurs during the first three years
of life but may rarely occur in adults. It may attain an enormous size,
nearly filling the abdomen. Quite
The tumour, which commences in the cortex, is 2 grey, soft and has a homogeneous character of a sarcoma. It tends to destroy the whole kidney and may spread to neighbouring organs. Distant metastases by the blood stream are not frequent.
The microscopic appearance varies in different parts of the same tumour. The general character is sarcomatous. The cells may be round or fusiform. Glandular elements are often present; smooth muscle and striated muscle are not uncommon and in rare cases there may be cartilage and bone.
A. Abnormalities in the amount of renal tissue
3. Large kidney
4. Supernumerary kidneys
B. Abnormalities of position, form and orientation
1. Displacement of kidneys
2. Horseshoe kidney.
C. Cystic diseases.
1. Bilateral agenesis of kidneys is incompatible with life and is found only in still-born babies.
2. Unilateral agenesis is compatible with adequate renal function. The other kidney is enlarged in size.
1. Unilateral absence of nephrogenic primordium.
Renal hypoplasia means the failure of the kidney to attain the normal
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