Understanding Kidney Diseases by Hugh C. Rayner Mark Thomas & David Milford

Author:Hugh C. Rayner, Mark Thomas & David Milford
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

All three criteria must be met to make a diagnosis of nephrotic syndrome. Low serum albumin and oedema without albuminuria can be found in many conditions. For example, chronic liver disease causes oedema due to salt retention and low serum albumin due to reduced synthesis. Systemic inflammation reduces serum albumin by depressing its rate of synthesis and increasing its breakdown. For this reason, serum albumin is described as a negative acute-phase reactant .

The oedema in nephrotic syndrome is commonly put down to reduced oncotic pressure from the low serum albumin allowing salt and water to leak into the tissues. However, this traditional explanation is not the full story [16]. For example, adults with congenital analbuminaemia , an autosomal recessive disorder where serum albumin is absent, have a low plasma oncotic pressure but little or no oedema.

The oedema of nephrotic syndrome is actually caused by retention of sodium by the kidneys combined with increased permeability of the capillary walls allowing fluid to leak into the tissues. Children with nephrotic syndrome that responds to steroid treatment excrete the excess sodium as soon as the proteinuria stops and before the serum albumin recovers.

Because the tubules are reabsorbing sodium along much of the length of the nephron, diuretics given at usual doses are often ineffective in nephrotic syndrome. Much higher doses of loop diuretics, sometimes in combination with a thiazide diuretic , are needed to block sodium reabsorption along a sufficient length of the nephron to achieve a diuresis (see Fig. 7.​3).

A renal biopsy is often performed to identify the pathological features of the nephrotic syndrome. An abnormality in all patients is fusion of the podocyte foot processes (Fig. 11.19). The digits of the podocyte merge across the slit diaphragm to form a continuous layer over the surface of the glomerular basement membrane. The width of the basement membrane is increased, suggesting that the collagen protein molecules are packed less tightly together, allowing protein molecules to pass between them. These changes are only visible under the electron microscope. Under light microscopy the specimen may show no definite abnormalities, in which case it is called minimal change nephrotic syndrome .

Fig. 11.19Electron micrograph showing complete fusion of the podocyte foot processes and thickening of the glomerular basement membrane in a patient with minimal change nephrotic syndrome. The average width of a normal membrane is 280 nm. Magnification 9300×

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