UMLS:C0035078 - FACTA Search

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Query: UMLS:C0035078 (renal failure)
31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelin (ET) is a powerful vasoconstrictor peptide synthesized and secreted by the vascular endothelium. Significant amounts of ET are also produced by nonendothelial cells, mainly tubular-epithelial and mesangial cells. Large amounts of ET are found in the urine compared with the small amounts present in blood. Because most of the ET filtered from plasma is subject to degradation by neutral endopeptidase (EC 3.4.24.11) in the proximal tubule, urinary ET is probably of renal origin. The range of urinary ET excretion in healthy persons is 20 to 90 ng/day. The excretion of endothelin is modulated by several mechanical and chemical stimuli such as angiotensin II, phenylephrine, radiocontrast media, cyclosporine, and cis-platin. In addition, enhanced urinary ET excretion has been found in several forms of renal failure, both acute and chronic, and in diabetes mellitus. Thus, urinary ET has the potential of serving as a marker for renal disease.
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PMID:Urinary endothelin: a possible biological marker of renal damage. 813 95

The agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) is an established nephrotoxicant in male Fischer 344 rats at i.p. doses of > or = mmol/kg. Since gender differences often exist in the susceptibility to toxicants, the nephrotoxic potential of NDPS was examined in female Fischer 344 rats. Rats (4-5/group) were administered NDPS (0.1, 0.2, 0.4, or 1.0 mmol/kg, i.p.) or vehicle (sesame oil, 2.5 ml/kg) and renal function monitored for 48 h. At a dose of 0.1 mmol/kg, NDPS had no effect on renal function. However, administration of NDPS at a dose of 0.2 or 0.4 mmol/kg resulted in marked nephrotoxicity characterized by diuresis, increased proteinuria, glucosuria, hematuria, elevated blood urea nitrogen (BUN) concentration and kidney weight, decreased organic ion accumulation and proximal tubular necrosis. NDPS treatment of 1.0 mmol/kg resulted in oliguric renal failure rather than polyuric renal failure in 3 of 4 rats. Proximal tubular damage was observed primarily in the S3 segment of the proximal tubule in NDPS-treated female rats, while in male rats the S1 and S2 segments are the initial renal targets. These results demonstrate that female Fischer 344 rats are more susceptible to NDPS nephrotoxicity than male Fischer 344 rats and that the site of the renal lesion is gender dependent.
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PMID:Acute N-(3,5-dichlorophenyl)succinimide nephrotoxicity in female Fischer 344 rats. 816 Jan 97

The early distinction between prerenal azotemia, characterized by an avid proximal tubular sodium reabsorption, and ATN, in which proximal tubule function is depressed, remains an important but difficult clinical task. Indices of acute renal failure based on urinary sodium excretion may be helpful but have several limitations, among which is the use of diuretics. The effectiveness of the fractional excretion of uric acid (FEUA) and that of endogenous lithium (FELi) in the diagnosis of acute renal failure has been evaluated in an unselected group of 46 patients, 28 with prerenal azotemia and 18 with ATN. In the entire group, FELi concurred with the clinical diagnosis in 78% of the patients, whereas the fractional excretion of sodium (FENa) and FEUA were in agreement in only 63 and 50%, respectively. FELi was more sensitive to identify hemodynamic renal failure, because 93% of prerenal failure patients had a low FELi, contrasting with a low FEUA in only 68% and a low FENa in 75%. The major reason for the discrepancy between FENa and FELi was the administration of diuretics. In both acute renal failure groups, FENa was higher in the subgroups receiving diuretics. In contrast, diuretic therapy had no effect on FELi in either group. These results suggest that FELi is more accurate than either FENa or FEUA for distinguishing prerenal azotemia from ATN. The superiority of FELi appears especially relevant in patients treated with the usual diuretics.
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PMID:Fractional excretion of trace lithium and uric acid in acute renal failure. 816 25

In order to evaluate tubular damage in diabetic patients, the activity of renal proximal tubule derived enzymes excreted in 24-hour urine were recorded in 5 groups as follows: (i) 48 noninsulin-independent diabetic patients with normal renal function and a urinary albumin excretion rate within the normal range; (ii) 45 noninsulin-dependent diabetic patients with normal renal function and a high urinary albumin level; (iii) 26 noninsulin-dependent diabetic patients with renal failure; (iv) 40 patients with essential hypertension and normal renal function, and (v) 48 normal control subjects. Regardless of whether cases were noninsulin-dependent diabetics with normal or high urinary albumin excretion rate or cases with renal dysfunction, urinary dipeptidyl aminopeptidase IV and N-acetyl-beta-D-glucosaminidase excretions were significantly higher than in healthy subjects, and urinary gamma-glutamyl transpeptidase excretion was significantly lower than in healthy subjects. No significant changes in urinary enzyme excretions showed specific variations in the essential hypertensive patients. These results suggest that there is tubular damage in the early stages of noninsulin-dependent diabetic patients with normal renal function and normal urinary albumin excretion rate. Detection of urinary excretion of dipeptidyl aminopeptidase IV, N-acetyl-beta-D-glucosaminidase and gamma-glutamyl transpeptidase may be especially useful for the early diagnosis of diabetic nephropathy.
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PMID:Diagnostic significance of urinary enzymes for diabetes mellitus and hypertension. 858 4

The limiting factor in the therapeutical use of cyclosporine A (Cs A) is its nephrotoxicity, which may lead to renal failure. Cs A nephrotoxicity may present itself as an acute decrease in GFR, or as a chronic renal injury. Nephrotoxicity is caused by the indirect vasoconstriction effect mainly on proximal tubule and afferent arteriols. In our study we have concentrated on the effect of Ca-channel blockers on Cs A nephrotoxicity. As parameters of toxic kidney damage we have used the urine levels of the following enzymes: N-acetyl-beta-D-glucosaminidase (NAG), gama-glutamyltransferase (GMT) and alkaline phosphatase (ALP). Daily intragastric application of verapamil (V) (dose 1.0 mg/kg BW) or nifedipine (N) (dose 0.1 mg/kg BW) was started in a group of male Wistar rats. Cs A (Sandimun Sandoz, Switzerland) was applied daily intraperitoneally 30 minutes after the application of V or N. The dose of Cs A ranged from 5 mg/kg BW to 25 mg/kg BW in individual groups. The animals were observed for 10 days after the drugs application. Urine samples were collected and examined at the end of the whole experiment. The individual parameters were evaluated in the groups receiving the 3 different doses of Cs A (5-25 mg/kg BW). The serum creatinine rose moderately during the experiment. When the Ca-channel blockers were administered, the rise was not as steep, but when the highest dose of Cs A was administered, the Ca-channel blockers did not influence the elevation of the serum creatinine. Using the standard dose of Cs A (5 mg/kg BW) the protective effect of Ca-channel blockers can be found. In higher doses of Cs A this protective effect was not expressed.
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PMID:The effect of calcium channel blockers on cyclosporine A (Cs A) induced nephrotoxicity in rats. 871 61

Mice deficient for B cell leukemia/lymphoma gene 2 [bcl-2(-/-) mice] manifest congenital renal hypoplasia and develop multicystic kidney disease and renal failure postnatally. To characterize postpartum renal development, to identify the cellular origin of the cysts, and to provide insight into the role that bcl-2 deficiency plays in the cystogenic process, we examined the morphology of kidneys from bcl-2 (-/-) mice and wild-type littermates [bcl-2 (+/+)] from birth (P0) to postpartum day 28 (P28), determined whether abnormalities of cellular proliferation and apoptosis accompany cyst development, and characterized expression of the bcl-2-related protein, bax. Between P0 and P7, kidneys from bcl-2 (-/-) and bcl-2 (+/+) mice undergo a comparable increase in weight and have similar histological appearances. However, during the next 2 wk of life, weight gain in kidneys from bcl-2 (-/-) mice is reduced compared with that in kidneys from bcl-2 (+/+) animals, and cysts develop in tubules with staining characteristics of proximal tubule, distal tubule/medullary thick ascending limb of Henle's loop, and collecting duct. Unaffected glomeruli and proximal tubules in kidneys of bcl-2 (-/-) mice undergo compensatory growth. Cystogenesis is accompanied by enhanced incorporation of 5-bromo-2'-deoxyuridine in cells within cortex and medulla and apoptosis of cells within cysts and in the renal interstitium. Bax protein is expressed in the distal tubule in kidneys of bcl-2 (+/+) and bcl-2 (-/-) mice and in some, but not all cysts. We conclude that abnormal regulation of DNA synthesis and apoptosis accompany cystogenesis in bcl-2 (-/-) mice during postpartum kidney development. Continued expression of bax could enhance apoptotic cell death.
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PMID:Abnormal postpartum renal development and cystogenesis in the bcl-2 (-/-) mouse. 876 Feb 59

Renal failure (RF) is a common accompaniment of multiple myeloma and is identified in over half of patients at presentation. RF is usually related to the presence of Bence-Jones protein (immunoglobulin light chain) which damages all the compartments of the kidney: glomerule, tubulo-interstitium and vasculature. The most common renal lesion is cast nephropathy, named "myeloma kidney": Cast are produced by two mechanisms: proximal tubule damage and intratubular cast formation. The predominant pathophysiologic mechanism of tubule damage appears to be a precipitation of Bence-Jones protein and Tamm-Horsfall glycoprotein produced by cells of ascending limb of Henle's loop in the tubule lumen. The therapeutic maneuvers to reduce renal damage and preserve renal function are reduction of plasma concentration of light chain with chemotherapy, elimination of factors which favour coprecipitation of Tamm-Horsfall protein with light chain (hypercalcemia, acid urine, radiocontrast material, furosemide, oliguria). At last, colchicine (1.2 mg/day) will also be efficacious in the acute management of patients with cast nephropathy.
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PMID:[Renal involvement in multiple myeloma. Physiopathology and therapy]. 881 49

The principal physiologic roles of the kidney are to maintain normal plasma volume and composition, to regulate calcium metabolism by controlling the synthesis of 1,25-dihydroxycholycalciferol (1,25-D3), to regulate hematocrit and to metabolize low molecular weight peptides. Alterations in protein metabolism result principally from losses of these functions. Metabolic acidosis causes increased skeletal muscle protein catabolism through regulated activation of the ATP-ubiquitinproteasome proteolytic pathway. Increased proteolysis is followed by oxidation of branch chain essential amino acids. Alanine and glycine released from muscle and glutamine and glutamate released from liver serve as substrate for renal ammoniagenesis, ultimately correcting acidosis. The cycle is subverted when kidneys are absent. Secretion of a variety of proteins is also perturbed. Hepatic secretion of insulin like growth factor-1 (IGF-I) in response to growth hormone is reduced. This in turn contributes to growth retardation, adding to the effects of acidosis. Muscle is also resistant to insulin in renal failure. Renal production of 1,25-D3 is reduced contributing to hyperparathyroidism, which in turn causes increased intracellular calcium in a variety of tissues contributing to decreased synthesis of immunoglobulins, mitogen-stimulated T-cell proliferation, and decreased glucose-stimulated insulin secretion. Hepatic synthesis of some proteins, such as apolipoprotein A-I and IGF-I are decreased, but synthesis of others, such as albumin, is normal. Low molecular weight peptides such as beta 2-microglobulin, normally filtered and catabolized in the proximal tubule, accumulate in plasma and may have deleterious effects.
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PMID:Derangements of protein metabolism in chronic renal failure. 889 32

The influence of angiotensin-converting enzyme (ACE) inhibition on renal tubular function in progressive chronic nephropathy was investigated in 69 patients by the lithium clearance (C(Li)) method. Studies were done repeatedly for up to 2 years during a controlled trial on the effect of enalapril on progression of renal failure. The pattern of proteinuria was followed over the first 9 months. At baseline, the glomerular filtration rate (GFR) was 5 to 68 mL/min. Absolute proximal tubular reabsorption rate of fluid (APR), estimated as the difference between GFR and C(Li), was 1 to 54 mL/min. Calculated fractional proximal reabsorption (FPR) was moderately subnormal. During the study, GFR decreased and sodium clearance was unchanged; fractional excretion of sodium therefore increased. In the group of patients randomized to treatment with enalapril (n = 34), GFR at 1 month was 83% (P < 0.001) and C(Li) was 88% (P < 0.01) of the baseline values, APR and FPR had not changed significantly, and potassium clearance was significantly decreased. Through the rest of the study period, APR remained nearly unchanged and FPR even increased in the enalapril group. In the group of patients randomized to treatment with conventional antihypertensive drugs (n = 35), C(Li) was unchanged until severe reduction in GFR, APR and FPR decreased gradually, and potassium clearance was almost unchanged. These differences in tubular function between the two treatment regimens were significant (P < 0.05). An unchanged or increased APR in either treatment regimen was associated with a long-term slower progression of renal failure. Over 9 months, the 24-hour fractional clearance of albumin decreased in the ACE inhibitor group (P < 0.01), whereas the clearances of immunoglobulin G and retinol-binding protein were unchanged in this group. In the conventional group, the fractional clearances of these three plasma proteins all increased. It is concluded that in progressive chronic nephropathy ACE-inhibitor treatment was associated with different adaptive tubular changes in the handling of sodium, water, and protein compared with conventional antihypertensive therapy. During ACE inhibition, the reabsorptive capacity of the proximal tubule appeared to be better preserved, which might be of importance for the beneficial effect of this treatment in chronic renal disease.
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PMID:The influence of angiotensin-converting enzyme inhibition on renal tubular function in progressive chronic nephropathy. 895 33

Neutral endopeptidase (NEP) is a 94 kDa ectoenzyme of the proximal tubule brush border, physiologically released into the urine with apical membrane fragments. As proximal tubular atrophy was a histological hallmark of Chinese herbs nephropathy (CHN), this study firstly determined renal excretion of NEP in healthy control subjects (N = 31), in patients with CHN (N = 26) and in women having consumed Chinese herbs and whose renal function was normal but running the risk of developing CHN (N = 27). Another patient group consisted of female patients with glomerular diseases (N = 12). At the same time, measurements of urinary microproteins (Clara cell protein, retinol binding protein, beta 2-microglobulin and alpha 1-microglobulin) were performed, as indicators of tubular dysfunction. Cell damage was estimated by the excretion of N-acetyl-beta-D-glucosaminidase (NAG). In the control group, the physiological NEP enzymuria was 43.1 micrograms/24 hr (geometric mean). In CHN patients, levels of urinary NEP were significantly decreased in those with moderate renal failure (26.7 micrograms/24 hr; N = 21; P < 0.05) and almost abolished in end-stage renal failure patients (4.35 micrograms/24 hr; N = 5; P < 0.05). In patients at risk as well as in patients with glomerular diseases, urinary NEP levels were not statistically different from those observed in control subjects (40.68 micrograms/24 hr and 48.5 micrograms/24 hr, respectively). Several degrees of tubular dysfunction and injury were noted in patients groups, as attested by increased urinary microproteins and NAG excretions. Considering the data from control and CHN patients, NEP enzymuria positively correlated with individual creatinine clearance values (r = 0.76; P = 0.0001) and negatively correlated with urinary microproteins levels (r = -0.55; P = 0.00001). Finally, NEP was regularly quantitated in the urine of 6 CHN patients for a period ranging from six months to two years and in 19 patients at risk during two years, respectively. In the first group, renal function progressively deteriorated in 3 patients, leading them to renal replacement therapy after 38 to 115 weeks. Stable parameters were observed in the remaining 3 patients. A direct correlation between creatinine clearance and NEP excretion was found longitudinally in each case. In the second group, no significant change of urinary NEP levels was observed (45.9 micrograms/24 hr), in parallel with stable renal function. Taken together, these results indicate that, in CHN patients, NEP enzymuria provides a rapid and noninvasive determination of the degree of structural impairment affecting the proximal tubular population and further reflecting the severity of the renal disease. The interest of this urinary marker in monitoring the progression of other tubulointerstitial diseases remains to be assessed.
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PMID:Proximal tubular injury in Chinese herbs nephropathy: monitoring by neutral endopeptidase enzymuria. 899 45

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