THE KIDNEY IN HEPATIC DISEASE AND IN GOUT: CLINICAL AND PATHOLOGIC ASPECTS

Abstract

Light microscopy and electron microscopy-studies of material obtained by renal biopsy on patients afflicted with disparate hepatic disease (acute hepatitis, biliary cirrhosis, Laennec''s cirrhosis, alcoholic liver, etc.) have shown the presence of abnormalities in all cases, even in the mildest ones. These consisted of deposition of osmiophilic granules, amorphous proteinaceous material and irregular black particles; later on, the mesangial matrix was increased, the basement membrane was thickened, and, in still more severe cases, capillary wall changes, with focal destruction of pedicels appeared. These anatomic changes probably form the substratum of the functional renal disturbances (occasionally even nephrosis) observed in the patients. The term hepatic glomerulosclerosis is suggested for these changes; hepatic nephropathy is the term suggested for the sudden renal failure observed in some of these patients; its mechanism is still unknown. Hyponat-remia, hypokalemia, oliguria, azotemia (frequently with normal creatinine levels) are frequently (but not always) observed. The prognosis is grave; the therapy is that of the hepatic disease. In gout the kidney is very frequently involved-especially in longstanding cases. The renal handling of urate, of amidotransferase, of pho-phoribosylpyrophosphate, of glutamine and of amino acid metabolism are all abnormal. About 10 - 30% of gouty patients die from renal insufficiency. Urate deposits are encountered and nephrolithiasis is quite common in gout. A distinct glomerulosclerosis has also been described. Uniform fibrillar thickening of the capillary basement membrane and an increased number of nuclei in the loops. Atrophy, dilatation and regeneration in Henle''s loops tubules, as also other changes similar to, but not identical, with chronic pyelonephritis, are also observed. Increased RNA content is apparently the main histochemical abnormality. Pathogenetically, the main problem is the hyperuricemia; that is why secondary "gout" is also encountered in leukemia and other diseases where high levels of uric acid are to be found. Apparently, gouty subjects recycle glutamine thus increasing uric acid synthesis. In other gouty patients only a normal turnover of uric acid was found, thus pointing to decreased reabsorption of this substance as the responsible mechanism. Clinically, proteinuria is the most common abnormality. Sooner or later, azotemia appears, sometimes reaching very high levels. There is no strict parallelism between the severity of arthropathy and nephropathy.