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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of acute NH4C1-induced metabolic acidemia on renal electrolyte excretion was examined in nine healthy subjects during steady state water diuresis. Following oral NH4C1, venous pH and bicarbonate concentration declined significantly (p less than 0.01) while inulin and PAH clearances remained unchanged. Mean sodium excretion (UNaV) increased from 142 +/- 16 mueq/min (mean +/- SEM) to 310 +/- 49 mueq/min (p less than 0.01) at 8 hr without change in plasma aldosterone or renin levels. Urine flow remained unchanged while CH2O/(CH2O + CCl) declined significantly, suggesting that acute metabolic acidemia inhibits sodium transport in the distal nephron. Similar results were observed in two subjects with central diabetes insipidus. Three subjects restudied following the ingestion of an equivalent amount of chloride administered as NaCl, failed to demonstrate a significant rise in UNaV. UKV fell acutely from 91 +/- 13 to 45 +/- 5 mueq/min (p less than 0.001) despite an increase in serum potassium concentration. No change in plasma insulin was observed. UCaV rose from 66 +/- 15 to 143 +/- 18 microgram/min and fractional excretion of calcium increased from 0.55 +/- 0.13 to 1.24 +/- 0.21% (p less than 0.001). Total serum calcium fell slightly, but ionized calcium rose from 3.99 +/- 0.05 to 4.30 +/- 0.03 mg/dl (p less than 0.001). No change in nephrogenous cyclic (cAMP) excretion was observed. In conclusion, acute metabolic acidemia in man (1) inhibits sodium reabsorption in the distal nephron independent of changes in plasma aldosterone concentration, filtered chloride load, or volume expansion; (2) inhibits potassium excretion despite a rise in serum potassium concentration; and (3) inhibits tubular calcium reabsorption independetn of changes in parathyroid hormone (as reflected by urinary cAMP).
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PMID:Effect of acute metabolic acidemia on renal electrolyte transport in man. 45 20

We have shown that the inhibition of prostaglandin (PG) synthesis in man decreases the fractional clearance of urea (FCurea). To understand the mechanism(s) by which PG affect the renal handling of urea, 6 normal volunteers were randomly studied in maximal antidiuresis (by water deprivation and by administering 1-desamino-8-D-arginine vasopressin) before and during PGE1 infusion, in two separate occasions: (A) after 7 days of normal protein (1 g/kg b.w./day) and water intake (10 ml/kg b.w./day), and (B) after 7 days of low protein intake (0.5 g/kg b.w./day) and high water intake (80 ml/kg b.w./day) to lower the corticomedullary osmotic gradient. During infusion of PGE1 at rates of 0.01, 0.05 and 0.1 micrograms/min/kg, randomly administered, the urinary fluid losses were replaced by infusing equal volumes of hypotonic NaCl (80 mmol/l). To evaluate the time effects of this protocol, control studies were performed in an other 8 subjects receiving vehicle infusion without PGE1. In study A, FCurea rose by 23% (p less than 0.01) at the lowest PGE1 infusion rate (0.01 micrograms/min/kg), in the absence of any simultaneous change in water and salt output, Uosm, PAH and inulin clearance. Higher PGE1 infusion rates (0.05 and 0.1 micrograms/min/kg) were associated with a progressive increase of FCurea (50%, p less than 0.001 and 91%, p less than 0.001, respectively), fractional clearance of water and salt output, inulin and PAH clearance and reduced Uosm from 1,005 (22 SEM; basal value) to 772 (38 SEM; minimum value) mosm/kg (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of urea tubular reabsorption by PGE1 infusion in man. 173 12

23 living related kidney transplant donors were prospectively studied to determine the degree of hyperfiltration which occurs after uninephrectomy and to monitor potential consequences of this procedure such as hypertension, microalbuminuria or renal functional impairment. Standard inulin and PAH clearance studies were performed immediately before (n = 23), one week after (n = 22) and one year after nephrectomy (n = 12). Hyperfiltration was defined as the ratio of (post-nephrectomy inulin clearance)/(0.5 x pre-nephrectomy inulin clearance), hyperperfusion was defined in an analogous way for PAH clearance. One week after uninephrectomy, hyperfiltration averaged 134 +/- 6% (SEM) and hyperperfusion was 138 +/- 6%. The degree of hyperfiltration did not correlate with donor age. One year after nephrectomy, hyperfiltration was nearly unchanged (130 +/- 7%) whereas hyperperfusion had significantly decreased to 119 +/- 8% (p less than 0.05). Blood pressure did not increase after nephrectomy and no new cases of hypertension were observed during follow-up. In contrast, there were two new cases of microalbuminuria at one week and one year after nephrectomy. Further follow-up of these kidney donors is warranted.
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PMID:[Glomerular hyperfiltration following unilateral nephrectomy in healthy subjects]. 175 67

Growth hormone is reported to increase renal plasma flow (RPF) and glomerular filtration rate (GFR) in some but not all studies. The discrepant results could be due to a delay in the effects of growth hormone on renal function. We therefore examined whether a growth hormone injection does increase RPF and GFR, whether this increase is delayed, and whether elevation in RPF and GFR is associated with increased plasma levels of insulin-like growth factor I (IGF-I). Seven normal adults received a single intramuscular injection of growth hormone, 0.15 mg/kg, and serial PAH and inulin clearances were then monitored for three consecutive days. Plasma growth hormone levels peaked an average of 2.25 hours after injection, at 128 +/- 12 SEM ng/ml, and then began to decrease; on the second day values were only slightly elevated and on the third day they were not different from baseline. Plasma IGF-I, analyzed by direct radioimmunoassay, did not change on the first day during 5.5 hours of measurements after injection. By the second day, plasma IGF-I was elevated to over twice baseline levels (P less than 0.05) and remained elevated on the third day (P less than 0.05). RPF and GFR did not change from baseline (546 +/- 19 and 100 +/- 3 ml/min/1.73 m2, respectively) during the 5.5 hours after injection on the first day.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The delayed effect of growth hormone on renal function in humans. 270 79

In patients with a nephrotic syndrome administration of prednisolone causes an increase of proteinuria. To elucidate the mechanism of this effect we have studied the acute proteinuric effect of prednisolone, 125 to 150 mg intravenously, in nine patients (7 M, 2F) with a nephrotic syndrome. Mean age (+/- SD) of the patients was 53 +/- 6 years, mean endogenous creatinine clearance 104 +/- 30 ml/min, and mean proteinuria 7.7 +/- 3.0 g/24 hr. After administration of prednisolone, urinary total protein excretion rose in all patients from a mean (+/- SEM) of 4.89 +/- 0.59 mg/min before to 9.09 +/- 0.99 mg/min at five hours after administration (P less than 0.01). Glomerular filtration rate (inulin clearance), effective renal plasma flow (PAH clearance), and filtration fraction did not change significantly. The increases of urinary excretion of albumin (median %: +92%), IgG (median %: +88%), and transferrin (median %: +76%) were comparable and correlated significantly. Urinary excretion of beta 2-microglobulin did not change significantly however. We conclude that intravenous administration of prednisolone to patients with a nephrotic syndrome causes an increase in urinary protein excretion rate which cannot be explained by changes in renal hemodynamics or tubular protein reabsorption, and which therefore must be the result of a change in glomerular permselectivity characteristics.
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PMID:Prednisolone can increase glomerular permeability to proteins in nephrotic syndrome. 340 15

Simultaneous renal clearances of inulin (CIN), p-aminohippurate (CPAH), and creatinine (CCR) were measured in hydrated mares (6 ponies and 2 horses). The CIN and CPAH were determined during steady-state infusion at 3 different infusion rates. A 6-fold change in plasma IN concentration did not produce alteration in CIN, nor was there a difference between the ponies and horses (P greater than 0.2). The overall average (mean +/- SEM) was 190.6 +/- 5.89 ml . min-1 . 100 kg of body weight-1. There was no difference noted between simultaneous CIN and CPAH. Clearance of PAH remained essentially constant during the change in plasma PAH from 0.33 mg/dl to 5.27 mg/dl. The extraction ratio of PAH for the nonanesthetized pony was 0.966. Effective renal plasma flow (CPAH) of the pony exceeded that of the horse.
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PMID:Renal function of the pony and the horse. 707 82

To characterize the role of the liver and kidney in the metabolic response to injury and infection, selective catheterization of the hepatic (42 veins) and renal veins (21 veins) was performed in 31 burn patients (mean burn size: 51% TBS), studied 4-129 days postinjury. Blood flow was determined by standard clearance techniques (ICG and PAH), and simultaneous arterial and hepatic and/or renal vein blood was obtained for oxygen, glucose, lactate, pyruvate, and amino acids. Patients studied in the first to third weeks postinjury were classified as noninfected (8 studies), bacteremic (8 studies), or bacteremic with complications (5 studies). There was no difference in age, weight, mean burn size, pulse rate, blood pressure, rectal temperature, total body oxygen consumption, or cardiac index among these groups. Estimated hepatic blood flow (EHBF) and hepatic substrate balance of these patients were compared with postabsorptive normal subjects in the literature (mean +/- SEM or range). :Formula: (See Text) Thermal injury alone resulted in marked increases in EHBF, hepatic oxygen uptake, and glucogenesis. The added insult of bacteremia significantly increased hepatic glucose output; as clinical sepsis progressed, glucose output decreased sharply. The kidney consistently demonstrated a net uptake of glucose in all studies. The changes in hepatic glucose output in bacteremic patients occurred without significant differences in EHBF, oxygen utilization or lactate uptake, but were associated with marked alterations in amino acid uptake.
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PMID:Effect of injury and infection on visceral metabolism and circulation. 742 96

Acute and chronic studies in rats have shown that administration of human recombinant insulin-like growth factor I (rhIGF-I) lowers renal vascular resistance and increases RPF, GFR and proximal tubular phosphate absorption. In the present study we examined the effects of subcutaneous injections of rhIGF-I on glomerular and tubular function in eight normal men. Individuals were studied for 5.5 consecutive days in a clinical research center while they ate a constant diet. Four subjects were studied in a non-volume expanded state (Group 1) and four individuals were evaluated during a saline load. From the second to the fourth day, subjects received subcutaneous injections of rhIGF-I, 60 micrograms/kg, at 0800, 1400 and 2000 hours. After commencing the rhIGF-I injections, serum IGF-I levels rose quickly and remained at about three to four times that of baseline throughout the period of rhIGF-I injections. In both the normal and the saline loaded subjects, renal vascular resistance decreased and RPF and GFR (PAH and inulin clearances) rose quickly and were clearly altered within six hours after starting the rhIGF-I injections. RPF had increased by 32 +/- 3% and 33 +/- 2% (grand mean +/- SEM) in the normal and the saline loaded subjects, and GFR rose by 22 +/- 3% and 36 +/- 4% in the two groups. In both groups the absolute and the fractional excretion of phosphate decreased markedly during rhIGF-I treatment, but the absolute and fractional excretion of calcium did not change. The urinary fractional and absolute excretion of albumin and IgG also increased, although slightly, with rhIGF-I injections. There was no consistent effect of IGF-I on tubular sodium handling. These findings demonstrate that in normal men subcutaneous injections of rhIGF-I greatly increase RPF, GFR, and tubular phosphorus reabsorption and enhances microproteinuria.
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PMID:Effects of insulin-like growth factor I on renal function in normal men. 844 Dec 34

Experimental and clinical studies have demonstrated a positive relationship between hyperlipidemia and rate of progression of renal disease, suggesting that lipids can induce or aggravate glomerular injury mainly by interacting with mesangial cells. Nevertheless, recently has been demonstrated that increased cholesterol levels can also induce endothelial cell dysfunction. Thus, since endothelium is known to play a major role in modulating the vascular tone, we have tested the possibility that hypercholesterolemia impairs the renal hemodynamics in patients with active nephrotic syndrome and elevated serum cholesterol levels. In this single-blind, nonrandom study, 12 patients were treated with pravastatin (group T, treated, n = 12) and 8 with placebo (group C, controls, n = 8). The controls were studied after the pravastatin group had been completed. Before starting the treatment the patients underwent basal determinations including routine laboratory investigations and PAH and inulin clearances. The same determinations were repeated after 48 h, and 6 and 12 weeks from the beginning of the treatment. The study at 48 h was performed to see if pravastatin had a direct, cholesterol-independent effect on renal function. The following basal results were reported (mean +/- SEM; group T vs. group C): serum cholesterol (mmol/l) 9.7 +/- 0.4 vs. 9.1 +/- 0.3 (NS); proteinuria (g/24 h): 6.2 +/- 0.2 vs. 7.0 +/- 0.7 (NS); PAH clearance (ml/min): 353 +/- 21 vs. 385 +/- 31 (NS); inulin clearance (ml/min): 62.5 +/- 7.7 vs. 67 +/- 9.3 (NS). After 48 h, no changes were observed in both groups. Subsequently, in group T, the following percentage changes of basal levels were observed: serum cholesterol -21.4 +/- 3.2% at 6 weeks (p < 0.05) and -34.9 +/- 3.2% at 12 weeks (p < 0.01); inulin clearance +3 +/- 3.7% at 6 weeks (NS) and +9.3 +/- 2.9% at 12 weeks (p < 0.05); PAH clearance +7 +/- 3.1% at 6 weeks (p < 0.05) and +21.2 +/- 5.5% at 12 weeks (p < 0.01). By contrast, no significant changes of these parameters occurred in group C at any time, so that the percent changes of baseline values of CPAH were significantly greater in group T (at 6 weeks: p < 0.05; at 12 weeks p < 0.005). These results indicate that the reduction of cholesterol is associated with a significant increase in renal plasma flow, thus, suggesting that hypercholesterolemia may actually impair the renal hemodynamics. We speculate that this effect may contribute to increase the risk of ischemic acute renal failure in nephrotic patients and, along with changes induced in the mesangium by other mechanisms, to contribute to the progression of renal disease.
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PMID:Effects of hypercholesterolemia of renal hemodynamics: study in patients with nephrotic syndrome. 883 3

In 16 African Americans (blacks, 14 men, 2 women) with average admission mean arterial pressure (MAP, mm Hg) 99.9+/-3.5 (mean+/-SEM), we investigated whether NaCl-induced renal vasoconstriction attends salt sensitivity and, if so, whether supplemental KHCO3 ameliorates both conditions. Throughout a 3-week period under controlled metabolic conditions, all subjects ate diets containing 15 mmol NaCl and 30 mmol potassium (K+) (per 70 kg body wt [BW] per day). Throughout weeks 2 and 3, NaCl was loaded to 250 mmol/d; throughout week 3, dietary K+ was supplemented to 170 mmol/d (KHCO3). On the last day of each study week, we measured renal blood flow (RBF) and glomerular filtration rate (GFR) using renal clearances of PAH and inulin. Ten subjects were salt sensitive (SS) (DeltaMAP >+5%) and 6 salt resistant (SR). In NaCl-loaded SS but not SR subjects, RBF (mL/min/1.73 m2) decreased from 920+/-75 to 828+/-46 (P<0.05); filtration fraction (FF, %) increased from 19. 4+/- to 21.4 (P<0.001); and renal vascular resistance (RVR) (10(3)xmm Hg/[mL/min]) increased from 101+/-8 to 131+/-10 (P<0.001). In all subjects combined, DeltaMAP varied inversely with DeltaRBF (r =-0.57, P=0.02) and directly with DeltaRVR (r = 0.65, P=0.006) and DeltaFF (r = 0.59, P=0.03), but not with MAP before NaCl loading. When supplemental KHCO3 abolished the pressor effect of NaCl in SS subjects, RBF was unaffected but GFR and FF decreased. The results show that in marginally K+-deficient blacks (1) NaCl-induced renal vasoconstrictive dysfunction attends salt sensitivity; (2) the dysfunction varies in extent directly with the NaCl-induced increase in blood pressure (BP); and (3) is complexly affected by supplemented KHCO3, GFR and FF decreasing but RBF not changing. In blacks, NaCl-induced renal vasoconstriction may be a pathogenetic event in salt sensitivity.
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PMID:NaCl-induced renal vasoconstriction in salt-sensitive African Americans: antipressor and hemodynamic effects of potassium bicarbonate. 1002 19


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