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W Suki

Publications and source records attributed to W Suki.

14 recordsLinked to original sources
PubMed1999

Neocytolysis contributes to the anemia of renal disease.

Neocytolysis is a recently described physiological process affecting the selective hemolysis of young red blood cells in circumstances of plethora. Erythropoietin (EPO) depression appears to initiate the process, providing the rationale to investigate its contributions to the anemia of renal disease. When EPO therapy was withheld, four of five stable hemodialysis patients showed chromium 51 (51Cr)-red cell survival patterns indicative of neocytolysis; red cell survival was short in the first 9 days, then normalized. Two of these four patients received oral 13C-glycine and 15N-glycine, and there was a suggestion of pathological isotope enrichment of stool porphyrins when EPO therapy was held, again supporting selective hemolysis of newly released red cells that take up the isotope (one patient had chronic hemolysis indicated by isotope studies of blood and stool). Thus, neocytolysis can contribute to the anemia of renal disease and explain some unresolved issues about such anemia. One implication is the prediction that intravenous bolus EPO therapy is metabolically and economically inefficient compared with lower doses administered more frequently subcutaneously.

Adult↗
PubMed1997

ASN at 30.

Explore the source record for details and available documents.

Cooperative Behavior↗
PubMed1994

Tenascin is an important component of the glomerular extracellular matrix in normal and pathologic conditions.

Tenascin (TN), a large oligomeric glycoprotein, is a recently described component of the extracellular matrix (ECM). Previous reports focusing largely on the role of TN in nephrogenesis have documented the strong expression of TN in embryonic kidney tissue and implied an important role for TN in nephrogenesis. However, the expression of TN in normal and pathologic kidneys in adults has not been systematically evaluated. In this study immunohistochemical staining for TN was applied to 184 renal specimens diagnosed as: normal kidney (23 cases); minimal change disease and its variants (8); mesangial proliferative glomerulonephritis (GN) including IgA nephropathy and mesangial proliferative lupus nephritis (9); endocapillary proliferative GN including membranoproliferative GN, lupus nephritis, and post-infectious GN (25); crescentic GN (11); membranous GN (19); focal segmental sclerosis (15); thrombotic microangiopathy (8); amyloidosis (5); diabetic nephropathy (9); primary tubulointerstitial nephritis (14); transplant rejection (14); and ischemia (24). It was found that: (a) there was unequivocal global diffuse staining limited to the mesangium in normal kidney; (b) regardless of the etiologies and the morphologic types of glomerular disease, whenever there was expansion of the ECM, whether in the mesangial, endocapillary, or extracapillary spaces, there was a concomitant and proportional in situ increase in the TN staining; (c) globally sclerotic glomeruli, regardless of causes, showed diffuse, strong staining, especially in the subcapsular fibrous deposition seen in ischemic sclerosis; (d) non-sclerotic glomeruli showing early ischemic change uniformly displayed a marked decrease or complete loss of staining; (e) in cases of thrombotic microangiopathy, there was segmental or global staining of the capillary wall, probably corresponding to the enlarged lamina rara interna; (f) all nodular lesions in diabetic glomerulosclerosis showed strong staining, but in several of them this staining was much more pronounced in the periphery than in the center of the lesion. Our study proves that TN is probably a component of the normal mesangial matrix, that TN is an ubiquitous component of the expanded glomerular ECM in pathologic conditions regardless of morphologic subtypes, and that further studies on the cell types and mechanisms responsible for TN synthesis may provide a new venue for the understanding of the process of glomerular sclerosis.

Absorption↗
PubMed1987

Primary renal lymphoma presenting as acute renal failure.

Diffuse bilateral infiltration of the kidneys by lymphoma cells is a rare but well-documented cause of acute renal failure (ARF). Only 51 such cases have been reported, 15 of which had ARF as the initial presentation of lymphoma. The clinical and pathologic features of these 15 cases and of two additional cases reported herein are reviewed. The diagnosis should be suspected in a patient with ARF, bilateral enlargement of the kidneys, minimal proteinuria, nonspecific findings on urinalysis, and absence of features of allergic tubulointerstitial nephritis. Renal imaging techniques may suggest the possibility of lymphomatous infiltration, but only renal biopsy or autopsy can provide a definitive diagnosis. Although modern chemotherapy and/or radiation therapy usually leads to a dramatic normalization of renal function, almost all patients eventually die of widespread recurrent lymphoma, despite the absence of clinical or pathologic involvement of the kidneys at the time of death.

Acute Kidney Injury↗
PubMed1975

Effect of diuretics on oxidative phosphorylation of dog kidney mitochondria.

An effect of diuretics on cellular metabolism has been shown. In order to examine further the direct effect of diuretics on renal mitochondria, their effect on isolated cortical (C) and outer medullary (OM) mitochondrial respiration was examined. Oxygen consumption rate (QO2) was measured in a Gilson oxygraph utilizing either glutamate-malate or succinate as substrate. QO2, expressed in nanoatoms of O2 per milligram of protein per minute, was always higher in C than OM: 140.7 +/- 2.8 VS. 121.2 +/- 2.4 (P less than 0.001) with glutamate-malate and 181.1 +/- 6.3 vs. 129.7 +/- 5.2 (P less than 0.001) with succinate. A dose-response curve was constructed for each of the following: sodium ethacrynate, furosemide, chlorothiazide, acetazolamide and chlormerodrin. All diuretics inhibited C and OM equally. The 50% inhibitory molar concentration for EA was 6.2 times 10(-4); for furosemide 1.5 times 10(-3); for chlorothiazide 8.1 times 10(-3); for acetazolamide 10.8 times 10(-3); and for chlomerodrin 3.1 times 10(-5). Neither cysteine nor dithiothreitol inhibited the effect of EA. The effect of chlormerodrin was abolished by cysteine. These results demonstrate that while a difference exists between C and OM mitochondria during control studies, each of the diuretics examined exerted an equal inhibitory effect on mitochondrial respiration from both C and OM. Mercurials are the most potent inhibitors and presumably exert their effect by reacting with sulfhydryl groups. They are followed in potency by ethacrynic acid, furosemide, chlorothiazide and acetazolamide.

Animals↗
PubMed1969

Renal concentrating mechanism: possible role for sodium-potassium activated adenosine triphosphatase.

Sodium-potassium activated adenosine triphosphatase activity was found to be almost twice as high in renal medulla as in cortex. Infusion of digoxin, a specific inhibitor of the enzyme, into one renal artery of the dog resulted in unilateral natriuresis, impaired concentrating capacity, and reduction of the enzyme activity in both cortex and medulla. It is suggested that the sodium-potassium adenosine triphosphatase plays an important role in urine concentration mechanisms.

Adenosine Triphosphatases↗