Oliguria

OLIGURIA (from the Greek oligos—small and ouron—urine), a reduction in the amount of urine excreted by the kidneys. Clinically, oliguria is observed relatively frequently, and it may be caused by various reasons located both within the kidneys themselves and outside them. However, a strict division of oliguria into renal and extrarenal is hardly possible, since in the very act of urination, renal and extrarenal factors are always inextricably intertwined. Predominantly renal forms of oliguria generally have a unified pathogenesis, which boils down to a deterioration of blood circulation in the renal glomeruli, or a drop in the filtration pressure within them. It is universally recognized that the excretion of water is carried out exclusively or mainly by the glomerular system; oliguria is, therefore, an expression of a profound or acute disturbance of their functions. This group includes oliguria in nephritis, nephrosclerosis, and cardiac congestion. Oliguria in the initial stage of acute glomerulonephritis serves as a typical symptom and occurs due to ischemia of the glomeruli or the formation of inflammatory exudate within them. No less characteristic is oliguria in cardiac congestion, when the kidneys are in a state of severe anoxemia and the blood pressure in the arterial limb of the capillary network falls. It should be noted that in these cases, other functions of the kidneys (salt and nitrogen excretion) may be preserved. Finally, upon the destruction of the vascular system of the kidneys in the final stage of their contraction—regardless of what caused it—oliguria sometimes replaces the preceding "compensatory" polyuria (see). Oliguria is observed, however, also in a number of diseases in which renal function is almost or not at all involved in the pathological process. Such are the so-called physiological oligurias observed after increased sweating or insensible perspiration (from prolonged walking, climbing a mountain), as well as oliguria in febrile patients. In such cases, oliguria is caused by a sharply negative water balance due to increased water loss via extrarenal pathways (through the skin and with exhaled air). Persistent oliguria is also observed during the retention of unusual amounts of salt in the blood and tissues (e.g., in myxedema, lobar pneumonia, in the stage of increasing edema, etc.). Oliguria is also observed after abundant fluid losses due to vomiting, diarrhea, or during the retention of significant amounts of fluid in the body (pyloric stenosis, formation of pleural exudates). Tissue retention of water in the liver also entails oliguria with the excretion of small portions of urine (opsiuria), which is observed in diffuse liver lesions (cirrhosis without ascites, acute yellow atrophy), as well as in splenomegaly. Many are inclined to see the cause of opsiuria in hepatic patients as a disturbance of the liver's regular role in water metabolism. Pick and his students have even described special mechanical sphincters in the hepatic veins, which in their opinion play the role of sluices (Venensperre) in the release or retention of water by the liver. This view is not generally accepted (see Metabolism, water), although the presence of oliguria in hepatic patients is clinically indisputably established. Standing apart are the relatively rare cases of persistent "primary" oliguria, which are extremely difficult to explain by any pathological-anatomical changes in the organs. Zondek links them to damage to the vegetative centers of water-salt metabolism, usually localized in the diencephalon. Sometimes such oliguria is combined with a number of other neuro-endocrine disorders (obesity, thermoregulation disorder), forming characteristic syndromes. Oliguria is usually a symptom of a disease, so the decision regarding its origin depends on the general clinical symptomatology of the case. In general, it should be taken into account that the presence of pathological components in the urine during oliguria (protein and especially erythrocytes) testifies to its renal origin. A normal qualitative composition of urine, on the other hand, rather characterizes oliguria of extrarenal origin. Treatment of oliguria boils down to the elimination of the underlying disease causing it (for example, nephritis, cardiac decompensation, etc.). One should strictly distinguish from oliguria various disorders of urination accompanied by a delay in the excretion of urine from the kidneys and bladder due to mechanical or neuro-reflex causes, as is the case with prostate hypertrophy, kinking of the ureter, etc. Lit.—see lit. to the articles Diuresis and Kidneys.