Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q92565 (GFR)
 4,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were performed to determine whether renal glutathione (GSH) is an important free-radical scavenger following ischemia and reperfusion, whether alterations in renal transport work affect renal GSH levels, and whether a decrease in renal work decreases susceptibility to postischemic renal injury via the first two effects. Following administration of either intravenous GSH to increase renal GSH or intraperitoneal diethylmaleate to decrease renal GSH, Sprague-Dawley rats underwent 60 minutes of renal ischemia. In animals with high renal GSH following GSH infusion, GFR 24 hours after ischemia was 0.43 +/- 0.08 ml/min compared to 0.15 +/- 0.02 ml/min in saline-infused control animals (P less than 0.01). When renal GSH was decreased by the administration of diethylmaleate postischemic renal dysfunction was accentuated. Twenty-four hours after ischemia GFR was 0.05 +/- 0.02 ml/min in diethylmaleate-treated animals and 0.28 +/- 0.06 ml/min in control animals (P less than 0.005). To test whether a decrease in renal transport work alters renal GSH the filtered load of sodium was reduced by producing unilateral renal artery stenosis. Alternatively, renal work was lessened when sodium reabsorption was interfered with by the infusion of a combination of natriuretic agents. Renal artery stenosis produced a 37% decrease in GFR. Renal GSH was 0.435 +/- 0.089 nmol/mg protein in intact kidneys and 0.804 +/- 0.239 nmol/mg protein in stenotic kidneys (P less than 0.05). The infusion of natriuretic agents produced no change in GFR or renal plasma flow but resulted in a striking elevation in renal GSH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal work, glutathione and susceptibility to free radical-mediated postischemic injury. 338 36

We examined in anesthetized dogs the effects of left (L) intrarenal artery infusion of angiotensin II (AII) on renal hemodynamics, urinary concentration and Na excretion, and papillary plasma flow (PPF) (measured by the albumin accumulation technique) in both kidneys. Following AII infusion (0.5 ng/kg/min) into the L renal artery, urinary Na excretion decreased and osmolality increased slightly ipsilaterally, whereas Na excretion did not change significantly and osmolality decreased in the right (R) kidney. PPF was significantly lower in the L compared to the R kidney. When saline loading was superimposed on L intrarenal AII infusion, there was a blunted natriuretic response ipsilaterally with a significantly smaller decrease in urine osmolality compared with the R kidney. PPF increased significantly in the R, but not in the L kidney. Finally, AII blockade with saralasin prior to AII infusion and saline loading prevented the differences between the two kidneys, including PPF. In all groups GFR and renal blood flow did not differ between the two kidneys before or after AII. These data suggest that AII regulates regional blood flow in the medulla, and that the exogenously administered AII induces papillary ischemia, which serves to preserve medullary hypertonicity, preventing an increase in PPF during saline loading, and possibly contributing to the diminished natriuretic response.
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PMID:Regulation of papillary plasma flow by angiotensin II. 343 Sep 49

We have studied the effect of cyclosporine A (CyA) in male Wistar rats with only one kidney, that had been subjected to 45 min of warm ischemia (IS + NX). The effects were compared with those obtained in rats with either one (NX) or two intact kidneys (2K). Vehicle treated rats that underwent the same surgical procedure served as controls. The GFR and the ERPF were determined during and after the treatment period. The CyA was administered i.m. daily for a period of 5 days a week for a period of 4 weeks. The dosages were 15, 30, or 60 mg/kg/day in the short-term study, and 15 mg/kg/day in the long-term study. With only 5 days of treatment, changes in the GFR induced by CyA were more pronounced in IS + NX rats when compared with NX rats. Furthermore, in contrast with NX rats, the GFR did not completely recover in IS + NX rats. During the 4 week treatment we found that in all 3 models the GFR was less in the CyA treated rats than in the vehicle treated rats. The degree of impairment of the GFR differed in the various models. At the end of the treatment period, the GFR of the CyA treated rats (expressed as a percentage of the vehicle treated rats) amounted to 84% in 2K rats, 64% in NX rats, and 46% in IS + NX rats. After cessation of the CyA administration, there was a complete recovery of the GFR to control levels in 2K and NX rats. In IS + NX rats, however, the GFR remained significantly below that of vehicle treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nephrotoxicity of cyclosporine A in rats with a diminished renal function. 351 23

Two distinct types of injury, cytoplasmic edema and cell fragmentation occur in the S3 segment of the proximal tubule in isolated hypoxic perfused rat kidneys (Krebs-albumin medium gassed without O2). The proportion of S3 tubules with fragmentation strongly correlated with the GFR and urine output during the perfusion, and approached 100% when the GFR was increased by high perfusion pressure. Conversely, the fragmentation lesion was absent and the edema lesion extensive when tubular transport was inhibited by perfusion with hyperoncotic medium to prevent glomerular filtration or by addition of ouabain (10(-2) M) to the perfusate. Polyene antibiotics increase membrane permeability and thus the work of active electrolyte transport. Perfusion with amphotericin (3 X 10(-5) M) or nystatin (200 U/mliter) in oxygenated medium also produced fragmentation in S3. The lesion was prevented in the non-filtering kidney. Ouabain completely eliminated the cell fragmentation due to nystatin and significantly reduced that due to amphotericin. These results suggest that the injury of cell fragmentation is enhanced by transport activity and diminished when transport is inhibited. The edema lesion appears fundamentally different and more akin to lesions described in ischemia where tubular flow is absent, active transport is diminished, and the morphologic changes appear related to loss of cell volume regulation. The type of hypoxic damage exhibited by proximal tubular S3 segments may therefore be conditioned by active ion transport of tubular cells.
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PMID:Transport-dependent cell injury in the S3 segment of the proximal tubule. 372 25

Many models have been developed to study renal function following injury. Two types of studies have evolved: acute--to define the acute renal injury and chronic--to determine the pattern of recovery. Current models allow either study alone to be performed, but they lack the flexibility to combine the studies. In this study of renal ischemia, a model was designed which solved this problem. The authors constructed a model for performing a unilateral nephrectomy and episiotomy on female dogs. Catheters were placed in the renal vein, vena cava, and aorta, and a renal artery flow cuff was applied. The catheters and wires were buried in a subcutaneous pocket and were exteriorized after a recovery of several weeks. The episiotomy allowed easy intermittent Foley catheterization. With the animals awake and in a harness, parameters of renal function were measured: renal extraction, filtration fraction, fractional excretion, osmolar clearance, and free water clearance. Glomerular filtration rate and renal plasma flow were calculated by inulin and paramino hippurate clearances. The animals were studied in diuretic and antidiuretic states. In addition, renal artery flow was determined by the Doppler flow cuff. All parameters were determined every half hour in the acute setting, then every day in the chronic setting. The model was easily reproducible and functioned well in the authors' renal ischemia studies. Initial experiments with 1 hour of warm ischemia produced a greater than 50 per cent reduction in GFR acutely. Chronic studies showed a GFR with a return toward normal. All model construction purposes and plans were met.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A new model to study acute and chronic renal failure. 378 43

Experiments were performed on 26 rats to evaluate the effect of furosemide and muzolimine in an experimental model of acute renal failure (ARF). After control clearance measurements from both the left and the right kidney, an acute hydronephrosis was produced on the left side only, to completely interrupt urine flow rate. At the 17th minute of stop-flow, placebo (4 animals), furosemide (4 mg i.v. in 5 animals) or muzolimine (1.2 mg i.v. in 5 rats) were injected and three minutes later the renal arteries were clamped bilaterally for 20 minutes. The arterial clamps and the left hydronephrosis were removed at the 20th minute of ischemia and then 5 consecutive clearance periods were performed from either side to assess recovery from post-ischemic ARF. There was no difference in the entity of GFR depression and speed of recovery of either kidney between placebo, muzolimine and furosemide. The left, post-hydronephrotic kidney consistently exhibited a post-ischemic renal function more depressed than that measured in the contralateral side, although the speed of recovery was the same. The ATP content of the renal tissue was significantly larger in the right kidney compared to the contralateral side in the group receiving furosemide. In the animals treated with muzolimine ATP was significantly depressed in both kidneys. In the post-ischemic period the urinary Na excretion and the fractional water excretion rose significantly with either diuretic compared to placebo. However, this did not influence the recovery in GFR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevention of acute renal failure by diuretics. 400 97

A twelve year old boy presented with sudden onset of severe hypertension and oligo-anuria. A diagnosis of Takayasu's Arteritis was made by aortography which demonstrated irregular narrowing of the lumbar aorta and renal arteries. Severe renal insufficiency necessitated maintenance hemodialysis. Hyperreninemic hypertension was intractable despite aggressive dialysis and multiple drug therapy. Renal biopsy after eight months of dialysis showed preservation of glomerular architecture. After nine months GFR improved spontaneously to 32 ml/min/1.73 m2 despite no improvement in his hypertension. This case report emphasizes the remarkable ability of renal parenchyma to recover function after sustained ischemia.
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PMID:Chronic renal failure due to Takayasu's arteritis: recovery of renal function after nine months of dialysis. 612 39

In the present study 1 h of total occlusion of the left renal artery in conscious rats was chosen as experimental model of ischemic acute renal failure (ARF), while the contralateral kidney was left intact. Chronic high dietary sodium intake, acute isotonic saline infusion, or administration of saralasin did not protect from ARF. Furosemide, mannitol, and verapamil converted oliguric into non-oliguric ARF in 100%, 75%, and 60% of the animals, resp. Protection from oliguria and preservation of GFR inversely correlated with the depression of cortical ATP-concentration (control: 1.32 +/- 0.07 mumoles/g wet weight) 6 h after ischemia by 16%, 41%, and 58% in mannitol- and verapamil- treated rats and in untreated rats, resp. At this time, Na-K-ATPase enzyme activities in renal cortex and papilla were unaffected, while enzyme activity in outer medulla was suppressed from 15.4 +/- 1.4 to 9.4 +/- 1.0 mumoles Pi/mg protein h in all groups of animals. The results suggest that in this model of ARF renal ischemia not only affects cellular energy supply in renal cortex but also causes severe structural and functional impairment in the outer medulla, probably leading to tubular obstruction and depression of glomerular function. Pharmacological protection from ischemic oliguric ARF cannot be achieved by prior induction of high urine flow rates alone but depends on the degree of metabolic and functional reserve of the injured tubular epithelium.
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PMID:Renal functional and metabolic studies on the role of preventive measures in experimental acute ischemic renal failure. 641

Experiments were performed using a variety of methods to assess the functional status of different nephron populations following 45 min of renal ischemia in the rat. Micropuncture techniques revealed that SNGFR and reabsorption in the surface nephrons are only modestly reduced after ischemia, whereas kidney GFR and reabsorption are more severely affected. Determinations of bolus velocity with the Hanssen technique or of glomerular blood flow with the microsphere method confirmed that both were highest in the surface nephrons, lower in the middle nephrons and lowest of all in the juxtamedullary nephrons after ischemia. It is concluded that surface nephron function is well-maintained following ischemia and that it is the functional deficiency of the deeper nephrons that is predominantly responsible for the impairment in whole kidney function. Although the pathogenic mechanism is not yet clear, neither tubular obstruction nor tubular leakage in the deeper nephrons seems to be involved. The present findings suggest that micropuncture of the surface nephrons is a technique of questionable validity for studying this type of acute renal failure, they explain the inability of the kidney to concentrate the final urine, and they predict a more pronounced deficiency in medullary than in outer cortical blood flow.
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PMID:Disparity between surface and deep nephron function early after renal ischemia. 662 Aug 50

Intrarenal blood flow, nephron function and whole kidney function were studied in the recovery phase of acute failure induced by 45 min of warm ischemia. Analyses were made 24 h, 7 days and 28 days after the ischemic insult. At 24 h the total renal blood flow was 4.0 ml . min-1 . g-1, decreasing to 1.2 within one week. After four weeks it was normalized to 3.4 ml . min-1 . g-1. The intrarenal blood flow distribution, studied with the 86-Rb extraction method, showed the same pattern of response, with no signs of a persistent heavy reduction in the deeper parts, as was found 10 min after recirculation (Karlberg et al. 1982 a). The contralateral, nonischemic kidney responded with hyperemia in all areas 24 h after the trauma, but after 7 days the values were normal. The function of the superficial nephrons was studied with the micropuncture technique. In the initial phase mainly obstructed nephrons were found, but after four weeks the nephrons were essentially normal. After 24 h the postischemic kidneys were anuric but at 7 days urine production had started and the GFR was 0.1 ml . min-1; this improved to 0.55 ml . min-1 after 4 weeks.
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PMID:Postischemic renal failure. Intrarenal blood flow and functional characteristics in the recovery phase. 713 94


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