[Clinical investigation of 10 cases with acute renal failure induced by neuroleptics].

It is well known that the myoglobinuric acute renal failure caused by drugs is an important clinical aspect of nephrology. On the other hand, neuroleptic malignant syndrome is an uncommon, but potentially fatal, idiosyncratic reaction to neuroleptics and is characterized by muscular rigidity, fever, autonomic dysfunction and altered consciousness. The most common serious complication of malignant syndrome is rhabdomyolysis. We investigated 10 cases with acute renal failure induced by haloperidol and other neuroleptics. At the time they developed acute renal failure, the patients were taking a wide variety of medications. However, seven of the patients who developed acute renal failure, had received haloperidol, phenothiazine and anticholinaergic drugs, and 2 cases with acute renal failure were taking lithium. Characteristic clinical manifestations of malignant syndrome were observed in 7 patients who had been administered haloperidol orally or intravenously. All of the patients with acute renal failure induced by haloperidol, lithium and other neuroleptics were treated successfully with blood purification therapy (HD or HDF). We concluded that acute renal failure associated with malignant syndrome evoked by haloperidol is an indication for blood purification therapy.

[High sensitive photometric assay of pancreatic lipase and clinical investigation of urinary lipase in patients with various histopathological types of primary glomerulonephritis].

We measured the activity of urinary lipase by high sensitive photometric method using 1,2-dirinoleoilglycerol as a substrate. Also, we investigated the clinical significance of the activity of urinary lipase in patients with chronic glomerulonephritis (GN) with special reference to the relation between the levels of the enzyme and histopathological changes of the kidney. Urinary activity of N-acetyl-beta-D-glucosaminidase (NAG) and urinary beta 2-microglobulin (BMG) were also measured to compare the difference of renal handling of these 3 substances. We could obtain the following results; 1) Good coefficient of correlation was observed between the activity of urinary lipase and the excretion of urinary BMG. 2) No correlation was observed between the activity of urinary lipase and the amount of urinary NAG in patients with chronic GN. 3) In some of the cases with secondary tubulointerstitial edema and inflammatory infiltration, the values of the activity of urinary lipase were markedly elevated. These results suggested that lipase was removed from the serum mainly by glomerular filtration and reabsorbed almost completely by tubular epithelial cells like the renal handling of BMG. In contrast, NAG secreted through the different renal metabolism in proximal tubule. The activity of urinary lipase might be a diagnostic marker for the secondary acute tubulointerstitial lesions in patients with chronic GN.

[Clinical investigation of urinary activity of NAG and AAP in patients with various types of primary glomerulonephritis].

We investigated the activity of NAG and AAP in the urine of 36 patients with chronic glomerulonephritis (GN) with special reference to the relation between the levels of the enzymes and histopathological changes of the kidney. The subjects consist of 7 cases of minimal change nephrotic syndrome (MCNS), 3 cases of membranous GN, 5 cases of IgA. GN, 5 cases of membranoproliferative GN, 3 cases of focal glomerulosclerosis and 12 cases of chronic renal failure who had creatinine levels of more than 2 mg/dl resulting from chronic GN. Urinary levels of NAG and AAP were significantly higher in cases with GN than those in cases with chronic renal failure. In cases with GN, urinary levels of NAG and AAP correlated with the amounts of urinary protein, while those levels had no correlation with the classification of histopathological changes of glomeruli. The high value of NAG/mg.protein ratio, NAG by urinary protein, might be explained by the degree of tublointerstitial damage. We concluded that urinary levels of NAG and AAP reflects the proximal tubular damage caused by protein reabsorption.