Immediate and early renal function after living donor transplantation.
(9/6121)
BACKGROUND: In order to assess the immediate renal function after living donor transplantation, renal function was compared in eight renal allograft recipients and their living related kidney donors during the first 24 h after transplantation. METHODS: Substantial and comparable intraoperative volume loading with Ringer's acetate and mannitol was performed together with the administration of frusemide. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were estimated by the clearances of inulin and p-aminohippurane, respectively. Tubular reabsorptive function and injury were estimated from the clearance of lithium, the fractional excretion of sodium and the urinary excretion of N-acetyl-beta-glucosaminidase. RESULTS: One hour after completion of surgery, GFR (54 +/- 7 ml/min) and ERPF (294 +/- 35 ml/min) were only 30% lower in the grafts than in the remaining donor kidneys, increasing to similar levels within 3 h. Only minor tubular dysfunction and injury were revealed in the grafted kidneys, and these tended to normalize within 24 h. CONCLUSIONS: By the present transplantation procedure comprising short ischaemia time and substantial volume expansion combined with mannitol and frusemide administration, kidneys from living donors regain nearly normal function within a few hours after transplantation. (+info)
P2 purinoceptor saturation by adenosine triphosphate impairs renal autoregulation in dogs.
(10/6121)
Recent studies have suggested a role for P2 purinoceptors on vascular smooth muscle cells in the mechanism of renal autoregulation. Experiments were performed in anesthetized dogs (n = 9) to examine renal blood flow (RBF) autoregulatory efficiency before and after saturation of P2 purinoceptors with acute intra-arterial administration of ATP (1 mg/kg per min). Dogs were pretreated with the nitric oxide synthase inhibitor nitro-L-arginine (NLA) (50 microg/kg per min), to avoid endothelial P2 receptor-mediated effects on nitric oxide release caused by the intra-arterial ATP infusions. NLA treatment decreased RBF (5.3+/-0.3 to 3.6+/-0.2 ml/min per g) and sodium excretion (3.6+/-0.4 to 0.9+/-0.2 ml/min per g) without producing significant changes in GFR (0.92+/-0.04 to 0.90+/-0.06 ml/min per g) or RBF autoregulatory efficiency. ATP administration to NLA-treated dogs resulted in further decreases in RBF (2.8+/-0.2 ml/min per g), GFR (0.58+/-0.05 ml/min per g), and sodium excretion (0.6+/-0.2 micromol/min per g). In addition, there was marked impairment of RBF autoregulatory efficiency during ATP infusion. The slopes of the arterial pressure-blood flow relationships at renal arterial pressures of >75 mmHg were significantly altered, from 0.003+/-0.001 to 0.2+/-0.002 ml/min per g per mmHg. Discontinuation of ATP infusion restored RBF autoregulatory efficiency. Norepinephrine (5 microg/kg per min) administration in these NLA-treated dogs decreased RBF (2.5+/-0.3 ml/min per g; n = 4) to a similar extent, compared with ATP, but did not impair RBF autoregulation. These results support the hypothesis that P2 purinoceptors may be involved in mediating autoregulatory adjustments in renal vascular resistance. (+info)
Renal function in high-output heart failure in rats: role of endogenous natriuretic peptides.
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The physiologic and pathophysiologic importance of natriuretic peptides (NP) has been imperfectly defined. The diminished renal responses to exogenous atrial NP in heart failure have led to the perception that the endogenous NP system might be less effective and thus contribute to renal sodium retention in heart failure. This study tests the hypothesis that in experimental heart failure, the renal responses to an acute volume load are still dependent on the NP system. The specific antagonist HS-142-1 was used to block the effects of NP in a model of high-output heart failure induced by an aortocaval shunt. Plasma cGMP levels and renal cGMP excretion were significantly lower in shunted and sham-operated rats receiving HS-142-1, compared with vehicle-treated controls, indicating effective blockade of guanylate cyclase-coupled receptors. Baseline sodium excretion and urine flow rate were lower in HS-142-1-treated sham-operated rats (15.2+/-1.1 microl/min versus 27.5+/-3.1 microl/min with vehicle, P < 0.001) and in HS-142-1-treated shunted rats (8.1+/-1.3 microl/min versus 19.9+/-2.3 microl/min with vehicle, P < 0.001). After an acute volume load, the diuretic and natriuretic responses were attenuated by HS-142-1 in control and shunted rats. The renal responses were reduced by HS-142-1 to a significantly greater extent in shunted rats than in control rats. HS-142-1 did not induce any significant systemic hemodynamic changes in either group, nor did it alter renal blood flow. However, the GFR in HS-142-1-treated shunted rats was lower than that in vehicle-treated shunted rats, both at baseline (0.6+/-0.3 ml/min versus 2.1+/-0.4 ml/min with vehicle, P < 0.05) and after an acute volume load (1.2+/-0.4 ml/min versus 2.6+/-0.4 ml/min with vehicle, P = 0.01), whereas no such effect was observed in control rats. These data indicate that the maintenance of basal renal function and the responses to acute volume loading are dependent on the NP system. The NP seem to be of particular importance for the maintenance of GFR in this model of experimental heart failure. These observations provide new insights into the importance of the renal NP system in heart failure. (+info)
Renal changes on hyperglycemia and angiotensin-converting enzyme in type 1 diabetes.
(12/6121)
Hyperglycemia causes capillary vasodilation and high glomerular capillary hydraulic pressure, which lead to glomerulosclerosis and hypertension in type 1 diabetic subjects. The insertion/deletion (I/D) polymorphism of the angiotensin I-converting enzyme (ACE) gene can modulate risk of nephropathy due to hyperglycemia, and the II genotype (producing low plasma ACE concentrations and probably reduced renal angiotensin II generation and kinin inactivation) may protect against diabetic nephropathy. We tested the possible interaction between ACE I/D polymorphism and uncontrolled type 1 diabetes by measuring glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) during normoglycemia ( approximately 5 mmol/L) and hyperglycemia ( approximately 15 mmol/L) in 9 normoalbuminuric, normotensive type 1 diabetic subjects with the II genotype and 18 matched controls with the ID or DD genotype. Baseline GFR (145+/-22 mL/min per 1.73 m2) and ERPF (636+/-69 mL/min per 1.73 m2) of II subjects declined by 8+/-10% and 10+/-9%, respectively, during hyperglycemia; whereas baseline GFR (138+/-16 mL/min per 1.73 m2) and ERPF (607+/-93 mL/min per 1.73 m2) increased by 4+/-7% and 6+/-11%, respectively, in ID and DD subjects (II versus ID or DD subjects: P=0.0007 and P=0.0005, for GFR and ERPF, respectively). The changes in renal hemodynamics of subjects carrying 1 or 2 D alleles were compatible, with a mainly preglomerular vasodilation induced by hyperglycemia, proportional to plasma ACE concentration (P=0.024); this was not observed in subjects with the II genotype. Thus, type 1 diabetic individuals with the II genotype are resistant to glomerular changes induced by hyperglycemia, providing a basis for their reduced risk of nephropathy. (+info)
Abnormal renal functions in cyanotic congential heart disease.
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Children with cyanotic congenital heart disease had a decreased glomerular filtration rate (71-8 +/- 18-9 ml/min per 1-73 m2) measured by endogenous creatinine clearances, compared with children who had had complete corrective surgery, children with noncyanotic heart disease, and normal children. There was a significant correlation between low glomerular filtration rate and haematocrit values above 50%. Daily urinary sodium excretion was reduced in the cyanotic patients. (+info)
Estimation of glomerular filtration rate from plasma creatinine concentration in children.
(14/6121)
The relation between the true plasma creatinine concentration (Pc) and the glomerular filtration rate corrected for body surface area (GFR/SA) was investigated in 108 individuals, and the following formula was derived: GFR/SA (ml/min per 1-73m2SA) = 0-43 Ht (cm)/Pc (mg/100 ml). This formula was tested in a second group of 83 children, and its accuracy and precision was compared to the 24-hour creatinine clearance. It was found to be superior to the creatinine clearance overall, and was as good, even if all results involving suspect 24-hour-urine collections were eliminated from analysis. The formula in SI usage is: GFR/SA (ml/min per 1-73 m2SA) = 38 Ht (cm)1Pc (mumol/l). (+info)
Hypotensive response to captopril: a potential pitfall of scintigraphic assessment for renal artery stenosis.
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A characteristic pattern seen on captopril renography is described that is due to systemic hypotensive response. Most patients with these findings on captopril renography do not receive renal artery angiograms in our clinic because it is usually recognized. However, this pattern has received little attention in the medical literature and may be misinterpreted as being due to physiologically significant renal artery hypertension. METHODS: Over the last 3 y, renal artery angiograms were performed on three patients with systemic hypotensive response pattern on captopril renography. This allowed a unique opportunity to correlate the results of the captopril renogram with the renal artery angiograms in this patient population. Captopril renography was performed with a glomerular filtration agent, diethylenetriamine pentaacetic acid (DTPA), and a tubular agent, o-iodohipurate (OIH). RESULTS: Renal artery angiograms showed no evidence of renal artery stenosis in three patients with systemic hypotensive response pattern on captopril renography. Systemic hypotension on captopril renograms results in preserved uptake of both DTPA and OIH and hyperconcentration in the cortex and collecting system. CONCLUSION: The systemic hypotensive response pattern seen on captopril renography is a distinctive pattern that does not represent physiologically significant renal artery stenosis. (+info)
Value of captopril renal scintigraphy in hypertensive patients with renal failure.
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The aims of this study were to show the value of captopril renal scintigraphy for detecting a renovascular cause in hypertensive patients with renal failure and to assess the ability to predict the beneficial effect of revascularization on renal function. METHODS: Thirty-eight patients with renal failure (mean glomerular filtration rate = 35 mL/min) underwent renal scintigraphy after injection of 99mTc-mercaptoacetyltriglycine. Baseline scintigraphy was performed, and the test was repeated 24 h later after oral administration of 50 mg captopril given 60 min before the test. RESULTS: In 5 of 6 patients with a renovascular cause for renal failure, and 2 of 3 patients with a probable arterial pathology, scintigraphy had a high probability. The result was indeterminate in the other 2 patients. In 5 of 11 patients with negative arteriography and 14 of 18 patients with probable absence of renovascular pathology, we found a low probability of functional renal artery stenosis. Six revascularization procedures were performed and were predictive of a beneficial effect in 5 patients. Time of peak activity was an effective predictor in each case. CONCLUSION: In hypertensive patients with renal failure, captopril renal scintigraphy can detect hemodynamic dysfunction downstream from a renal artery stenosis and can predict the beneficial effect of revascularization in some cases. (+info)