Diseases of the kidneys are divided into 5 major groups:

1. Glomerular diseases.

2. Tubular diseases.

3. Interstitial diseases.

4. Vascular diseases.

5. Tumours of the kidney.

There are two main types of partial renal failure: nephritic syndrome and nephrotic syndrome.

Nephritic syndrome is the result of disturbance of glomerular structure that involves reactive cellular proliferation. This causes reduced glomerular blood flow (leading to reduced urine output — oliguria), leakage of red cells from damaged glomeruli (hematuria), and consequent retention of waste products (uremia). The low renal blood flow activates the renin-angiotensin system, with fluid retention and mild hypertension. Small amounts of proteins are also lost in the urine, but this is usually trivial. The hematuria is not gross and is usually manifested as a smoky brown discoloration of urine.

Nephrotic syndrome is the result of abnormality in glomerular basil membranes or mesangium, such

that the glomerulus loses the capacity for selective retention of proteins in the blood. This leads to loss of very large amounts of protein, mostly albumin, in the urine (proteinuria), with consequent loss of protein from the blood (hypoalbuminemia) leading to edema. Other indications of renal abnormality are intermittent hematuria and persistent proteinuria which can be thought of as early partial renal failure. The latter may precede the development of a nephrotic syndrome.


Acute renal failure is characterized by widespread abrupt cessation of nephron function. Acute renal failure is a form of total renal failure in which the majority of nephrons suddenly and simultaneously stop working.

The causes of acute renal failure may be pre-renal (e.g., inadequate cardiac output and hypovolemia or vascular disease causing reduced perfusion of the kidney), intra-renal (e.g., rapidly progressive glomerulonephritis, acute tubular necrosis, pyelonephritis), post-renal (e.g., caused by a mass, within the lumen, or from wall of the tract, or from external compression).

Clinically this causes a dramatic fall in urine production (oliguria), which is often total (anuria). With little opportunity for metabolic compensation, problems of disturbed fluid and electrolyte balance and

failure of elimination develop rapidly. There is an increase in serum potassium level and metabolic acidosis, and nitrogen retention with uremia. Several diseases can produce acute renal failure, all of which cause sudden generalized cessation of nephron activity.


Chronic renal failure is a form of total renal failure caused by progressive destruction of individual nephrons over a long period of time.

The disease leading to chronic renal failure can generally be classified into two major groups: those causing glomerular pathology, and those causing tubulo-interstitial pathology.

The important examples of chronic glomerular diseases causing chronic renal failure are primary and systemic. Primary glomerular pathology are chronic glomerulonephritis, lipoid nephrosis (minimal change disease) and anti-glomerular basement membrane nephritis. Major examples of systemic glomerular pathology are systemic lupus erythematosus, serum sickness nephritis and diabetic glomerulosclerosis.

Tubulointerstitial diseases can be classified according to initiating etiology into 4 groups: vascular (e.g., primary or essential hypertension), infectious (e.g., chronic pyelonephritis), toxic (e.g., intake of high doses of analgetics such as phenacetin, aspirin and acetaminophen) and obstructive (e.g., stones, blood clots, tumours, strictures).

As more and more nephrons are destroyed, renal function becomes progressively more impaired. However, in contrast to acute renal failure there is opportunity for metabolic compensation. The latter produces early inability to concentrate urine (polyuria) and abnormalities in biochemical homeostasis (including salt and water retention, compensated metabolic acidosis, and other electrolyte imbalances, particularly hyperkalemia). Sodium and fluid retention may cause hypertension.

In contrast to many cases of acute renal failure, chronic renal failure is not reversible because there has been destruction of nephrons. A kidney in which all nephrons have been irreversibly damaged is macroscopically small and shriveled and is known as an end-stage kidney.


The term glomerulonephritis is traditionally used to describe the group of diseases in which the primary pathology is some sort of structural abnormality in the glomerulus. Despite the suffix «-itis», most are not characterized by inflammatory changes. Damage to the glomerulus may be severe, leading to permanent scarring, in which case the associated tubule atrophies. Alternatively, some conditions produce temporary abnormality and, following resolution, there is restoration of nephron function.

Principles of glomerulonephritis classification. Glomerulonephritis may be primary or secondary. According to the etiology it may be bacterial, viral, unclear. According to the pathogenesis there are 2 types of glomerulonephritis — immunoassociated and non-immunoassociated. According to the course glomerulonephritis may be classified into acute, subacute, chronic. In morphological classification, topography, character, propagation of pathological process are accounted.

Glomerular disease is classified according to the histological pattern of damage seen on renal biopsy, hence a knowledge of this aspect of histopathology is needed to understand disease. This arrangement is supplemented by further classification according to etiology of disease.

Morphology. Five main patterns of response to damage are seen in the glomerulus, combinations of which describe all types of glomerular disease.

1. Proliferation of endothelial cells leads to occlusion of capillary lumina, often with neutrophils present. This proliferation reduces the flow through glomeruli and correlates with oliguria and uremia.

2. Proliferation of mesangial cells, which is usually associated with increased production of matrix, is a common feature of many glomerular diseases. In some cases this may regress once the acute episode is over, in others the production of excess mesangial matrix over many years eventually leads to sclerosis

(hyalinization) of all or part of the glomerular tuft, with loss of capillary lumina.

3. Basement membrane thickening may be due to the deposition of an abnormal substance (immune complexes or amyloid), synthesis of new basement membrane material, insinuation of mesangial cytoplasm and matrix, or a combination of these causes.

4. Capillary wall necrosis, usually fibrinoid necrosis, occurs in diseases in which there is severe acute capillary wall damage, e.g. necrotizing vasculitis and accelerated (malignant) hypertension.

5. Crescent formation is an important reaction to severe glomerular capillary damage, stimulated by leakage of blood and fibrin into the urinary space. Crescents are formed by proliferation of the epithelial cells that line the Bowman's capsule, which crush the glomerulus, and lead to permanent loss of the whole nephron. The presence of widespread crescents is a poor prognostic sign, relating to severe and usually rapidly progressive disease.

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