Nephrotic Syndrome and its Serious Effects

Urine examination shows critical abnormalities in nephrotic syndrome. The urine may froth if passed in a container or if shaken in a test tube. The dipstick test always shows extensive excretion of protein in urine. Total excretion of protein per day should be measured in 24-hour's collection of urine. The nephrotic syndrome is the consequence of prolonged massive proteinuria (excretion of protein in urine). The proteinuria exceeds 3.5 g/24-hours in adults or 50 mg/kg body-weight in children. Nephrotic syndrome is characterized by proteinuria, hematuria (blood in urine), hypertension (high blood pressure), oliguria (low output of urine per day), edema (swelling: apparently suborbital puffy eyes) and diminished renal function. Urine may be brown or red. Sodium (Na⁺) retention, increased circulating blood volume and hypertension (high blood pressure) may lead to cardiomegaly (enlargement of heart). Nephrotic syndrome is usually characterized by insidious onset of massive edema, proteinuria, hypoalbuminemia (low level of albumin in blood) and hyperlipidemia (high level of cholesterol in blood). There could be massive retention of sodium (Na⁺) and a tendency to excessive potassium (K⁺) loss. Serious ill effect of the nephrotic syndrome could be a tendency towards hypercoagulability (blood clotting disorder) which may lead to venous or arterial thrombosis and embolism. Susceptibility to chest (lung) infections may increase due to decreased immunoglobulins' level in blood. Serum calcium (Ca⁺⁺) level could be low as this is related to the level of albumin in blood. Dysfunction of proximal tubules of kidneys may cause glycosuria (excretion of glucose/sugar in urine) or aminoaciduria.

How Hypertension Is Related To Kidney

High blood pressure or hypertension is one of the most characteristic phenomenon of chronic glomerulonephritis. It is evident that renal lesions (pathological abnormality in kidney) of an ischemic kidney (kidney with poor blood supply) may cause hypertension. This has been seen in the secondary hypertension which develops in the course of glomerulonephritis. Mechanical as well as pathological compression of renal parenchyma has been found to cause hypertension in experimental animals. Chronic pyelonephritis may also cause hypertension.

A variety of renal disorders (kidney diseases) may give rise to hypertension. The kidney disease may be parenchymal or of vascular origin primarily. Morbid anatomical studies have revealed that partial occluding of even one of the renal arteries due to intimal thickening (thickening of internal lining of artery) could be a cause of hypertension due to renal involvement. The vascular or presser substance can be formed by an ischemic kidney. Healthy kidneys are capable of eliminating any presser substance formed in the system. The circulating presser substance is called hypertensin or angiotonin. The angiotonin is formed in the blood by the interaction of an enzyme, renin, secreted by ischemic kidney. The maintenance of normal blood pressure depends on a correct balance between the production of a presser material by the adrenal cortex and its removal by the kidneys. The hypertension may be the result of over-activity of the adrenal gland or some renal disorder.

The primary hypertension and the renal hypertension could be ruled out by the family physician of the patient. In the primary hypertension, the high blood pressure develops early without any renal insufficiency, but in glomerulonephritis, the hypertension develops gradually with renal insufficiency and anemia (fall in hemoglobin level in blood). However, if the patient is seen only after the development of uremia (high level of urea in blood) making distinction between the primary or secondary hypertension could be difficult.