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At least 649 records · Page 36Linked to original sources
PubMed1992

Amelioration of ischemic acute renal failure by dietary fish oil administration in conscious dogs.

The hypothesis that dietary fish oil would protect dogs from ischemic acute renal failure was tested. Fish oil (eicosapentaenoic acid, 55 mg/kg per day, and docosahexaenoic acid, 40 mg/kg per day was given to eight instrumented, female, beagle dogs for 6 wk, while seven control dogs received vehicle. After 3 wk, unilateral nephrectomy was performed and a pneumatic cuff with flow probe was placed around the remaining renal artery of each dog. Three weeks thereafter, the cuff was inflated for 120 min. Renal function, RBF, and prostanoid excretion were measured 24 and 72 h after ischemia. In dogs receiving fish oil, blood pressure, GFR, RBF, renal vascular resistance (RVR), cholesterol, triglycerides, and prostanoid excretion were measured weekly for 6 wk. Further, cytosolic calcium was measured before and five times after fish oil. Blood pressure decreased, serum cholesterol and triglycerides decreased, and the cytosolic calcium within platelets decreased. The urinary excretion (expressed as picograms per milligram of creatinine) of the thromboxane (TX) metabolite TXB2 and the excretion of prostaglandin (PG)E2, as well as the excretion of the PGI2 metabolite 6-keto PGF1 alpha were decreased. GFR, RBF (Cl inulin and Cl para-aminohippuric acid), and RVR were not influenced by fish oil. Unilateral nephrectomy decreased GFR and RBF and increased RVR as expected, whereas it further decreased prostanoid excretion. Acute renal ischemia caused a significant, reversible decrease in GFR and urine volume in vehicle-treated animals, whereas no significant effect on renal function or urine volume was observed in animals pretreated with fish oil.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1984

[Work of the active transport system of organic acids in the kidney proximal tubules of rats with compensatory hypertrophy].

The active transport of organic acids in proximal renal tubules of the Campbell, Wistar and random-bred rats was studied by contact microfluorometry with anion dye fluorescein as a marker, on 1, 2, 3, 5, 10, 30 and 90 days after a unilateral nephrectomy. Sham-operated rats were used as a control. Transport was investigated under certain conditions when fluorescein was transported by Na-dependent (at 30 degrees C) or Na-independent (at 20 degrees C) systems. It is shown that fluorescein accumulation in renal tubules of operated random-bred rats at 30 degrees C is (if compared to the corresponding control) 81, 105 and 75% on 1, 2 and 3-10 days, resp., and about 90% on 30 and 90 days. Fluorescein accumulation at 20 degrees C in all investigated rats was about 90% of the corresponding control. A specific poison of Na+, K+-ATPase = ouabain inhibited fluorescein accumulation on day 1 after sham-operation by 70% to control, but there was no inhibition on day 1 after the operation (unilateral nephrectomy). P-aminohippuric acid in both media inhibited fluorescein accumulation in renal tubules of sham-operated rats better than in operated rats. It is concluded that either the amount of the carried of transport system for organic acids decreased in membranes of renal tubules of operated rats, or the affinity of carrier to organic acids is aggravated.

Acids↗
PubMed1999

Carrier-mediated uptake of lucifer yellow in skate and rat hepatocytes: a fluid-phase marker revisited.

Uptake of lucifer yellow (LY), a fluorescent disulfonic acid anionic dye, was studied in isolated skate (Raja erinacea) perfused livers and primary hepatocytes to evaluate its utility as a fluid-phase marker in these cells. However, our findings demonstrated that LY is transported across the plasma membrane of skate hepatocytes largely via carrier-mediated mechanisms. Isolated perfused skate livers cleared 50% of the LY from the recirculating perfusate within 1 h of addition of either 22 or 220 microM LY, with only 4.5 and 9% of the LY remaining in the perfusate after 7 h, respectively. Most of the LY was excreted into bile, resulting in high biliary LY concentrations (1 and 10 mM at the two doses, respectively), indicating concentrative transport into bile canalicular lumen. LY uptake by freshly isolated skate hepatocytes was temperature sensitive, exhibited saturation kinetics, and was inhibited by other organic anions. Uptake was mediated by both sodium-dependent [Michaelis-Menten constant (K(m)), 125 +/- 57 microM; maximal velocity (V(max)), 1.5 +/- 0.2 pmol. min(-1). mg cells(-1)] and sodium-independent (K(m), 207 +/- 55 microM; V(max), 1.7 +/- 0.2 pmol. min(-1). mg cells(-1)) mechanisms. Both of these uptake mechanisms were inhibited by various organic anions and transport inhibitors, including furosemide, bumetanide, sulfobromophthalein, rose bengal, probenecid, N-ethylmaleimide, taurocholate, and p-aminohippuric acid. Fluorescent imaging techniques showed intracellular vesicular compartmentation of LY in skate hepatocyte clusters. Studies in perfused rat livers also indicated that LY is taken up against a concentration gradient and concentrated in bile. LY uptake in isolated rat hepatocytes was saturable, but only at high concentrations, and demonstrated a K(m) of 3.7 +/- 1.0 mM and a V(max) of 1.75 +/- 0.16 nmol. min(-1). mg wet wt(-1). These results indicate that LY is transported into skate and rat hepatocytes and bile largely by carrier-mediated mechanisms, rather than by fluid-phase endocytosis.

Animals↗
PubMed1989

Acute changes in renal function associated with deferoxamine therapy.

In three patients who received intravenous deferoxamine there was a twofold to eightfold increase in plasma creatinine level and a parallel decrease in creatinine clearance that resolved when treatment with the drug was discontinued. In two thalassemic patients, diuresis was evident by urine output exceeding fluid intake. The mechanism was studied in dogs that exhibited an acute and significant decrease in inulin and para-aminohippuric acid clearances induced by intravenous deferoxamine. Saline diuresis could prevent the decrease in the glomerular filtration rate but not the decrease in renal blood flow caused by deferoxamine. Deferoxamine induced an acute increase in the fractional excretion of sodium, potassium, chloride, phosphate, and urate, which may explain the relative diuresis observed in two of the patients. In a subsequent experiment, ferrioxamine induced an increase in the fractional excretion of sodium and chloride but did not affect the glomerular filtration rate and renal blood flow. Our studies suggest that adequate hydration may be needed to preserve renal hemodynamics during intravenous deferoxamine therapy. Repeated measurements of renal function should accompany treatment with this agent.

Adolescent↗
PubMedDate not supplied

Ifosfamide metabolite chloroacetaldehyde causes renal dysfunction in vivo.

Renal injury is a common side-effect of the chemotherapeutic agent ifosfamide. Current evidence suggests that the ifosfamide metabolite chloroacetaldehyde may be responsible for this nephrotoxicity. The present study examined the effect of increasing amounts of intrarenally infused chloroacetaldehyde on kidney function, glutathione content and malondialdehyde formation. The ability of the uroprotectant medication sodium 2-mercaptoethanesulfonate (mesna) to prevent chloroacetaldehyde-induced renal injury was also assessed. Intrarenal chloroacetaldehyde infusion caused dose-dependent declines in glomerular filtration rate and p-aminohippuric acid clearance and increases in urine flow rate, sodium, glucose and protein excretion. These abnormalities were associated with progressive kidney glutathione depletion and malondialdehyde accumulation. Mesna infusion did not affect renal function but did cause a significant fall in kidney glutathione content. Simultaneous administration of chloroacetaldehyde and mesna only partially corrected renal functional abnormalities and prevented malondialdehyde accumulation but not glutathione depletion. These results show that the ifosfamide metabolite chloroacetaldehyde causes kidney dysfunction, glutathione depletion and lipid peroxidation in vivo. Mesna provides limited protection against chloroacetaldehyde nephrotoxicity, potentially explaining its inability to completely prevent ifosfamide-related renal injury in clinical practice.

Acetaldehyde↗
PubMed1989

Sulindac kinetics and effects on renal function and prostaglandin excretion in renal insufficiency.

The purpose of this study was to evaluate the pharmacokinetics of sulindac, a purported "renal sparing" nonsteroidal anti-inflammatory drug, and its effects on renal function and prostaglandin excretion in patients with reduced glomerular filtration rate. Twelve female patients (glomerular filtration rate 37 +/- 4 mL/min) were treated with sulindac 200 mg bid for 11 days. Urinary PGE2, 6-keto-PGF1 alpha and serum thromboxane (TxB2) generation were measured by radioimmunoassay (RIA) following extraction on C-18 columns. Glomerular filtration rate and effective renal plasma flow were measured by 99TC-DPTA and 131I-para-aminohippuric acid clearance. In six patients serum and urine levels of sulindac and its metabolites were measured by high-pressure liquid chromatography (HPLC). Sulindac was rapidly absorbed and converted to sulindac sulfide with peak levels 2 hours after a single dose, but steady state levels were not reached prior to drug discontinuation. Sulindac sulfide AUC (0-5 hours micrograms min/mL) progressively increased from 382 to 3,030 on day 11. It did not appear in the urine. Baseline urinary PGE2 and 6-keto-PGF1 alpha excretion were 23.8 +/- 5.6 and 18.9 +/- 2.7 ng/hr respectively and were reduced by 68% and 47% by day 4 of therapy. TxB2 generation fell by 34% after one dose and by 67% by day 11. There was a significant increase in serum creatinine from 1.88 +/- 0.13 mg/dl before treatment to 2.16 +/- 0.15 mg/dL (P less than .05) after eleven days.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1983

Regulation of a S(trans-1,2-dichlorovinyl)-L-cysteine-induced renal tubular toxicity by glutathione.

The nephrotoxin S-(1,2-dichlorovinyl)-L-cysteine (DCVC) is cleaved in the renal tubules to produce a reactive electrophilic intermediate. If this intermediate is responsible for the toxicity, addition of the nucleophilic scavenger glutathione (GSH) should decrease toxicity, and depletion of tubular GSH should enhance toxicity. GSH was added to isolated rabbit renal tubules simultaneously with, 15 min before, and 15 min after the addition of DCVC. The active accumulation of the organic anion para-aminohippuric acid (PAH) and organic cation tetraethylammonium bromide (TEA) was used as an index of renal toxicity. Incubation of renal tubules with 0.01-1 mM DCVC for 15 min decreased active transport, with complete inhibition at 1 mM. This was accompanied by a 50% decrease in non-protein sulfhydryl concentration. The addition of GSH (6 mM) simultaneously with DCVC completely prevented any decrease in active transport. The addition of GSH (6 mM) to tubules in which active transport was inhibited by DCVC reversed the inhibition to 80% of control. Similar enhancement of active transport occurred when tubules isolated 1 h after in vivo exposure to DCVC at 20-100 mg kg-1 were incubated with GSH (6 mM). Preincubation of renal tubules with GSH (5-15 mM) made them more refractory to the DCVC-induced decreased PAH and TEA transport. The inhibition of active transport by DCVC is enhanced if the tubular non-protein sulfhydryl is first lowered by diethyl maleate or glycidol. Thus, the tubular GSH concentration appears to be an integral component in regulating the alterations in active transport caused by DCVC.

Animals↗
PubMed1996

Influence of Ca2+ concentration on the clearance and circulating levels of intact and carboxy-terminal iPTH in pentobarbital-anesthetized dogs.

The role of hormone secretion and hormone clearance in the differential control of circulating levels of intact (I-) and carboxy-terminal (C-) immunoreactive parathyroid hormone (iPTH) was evaluated in 18 pentobarbital-anesthetized dogs. Catheters were installed in the aorta, left renal, and hepatic veins for sampling. Hepatic and renal blood flows were calculated from sulfobromophtalein (BSP) and p-aminohippuric acid (PAH) extraction and clearance. I- and C-iPTH were measured during a 1 h of infusion of CaCl2 or Na2EDTA. High-performance liquid chromatography (HPLC) profiles of I- and C-iPTH in and out of the liver and kidney were also obtained. Data on two dogs (one CaCl2 and one Na2EDTA infusion) were pooled for the analysis of one parathyroid function using a four-parameter mathematical model. Results obtained in the basal state and during analysis of the parathyroid function were also compared with those of 24 awakened dogs. Results are means +/- SD. Anesthetized dogs had lower levels of Ca2+ (1.29 +/- 0.03 vs. 1.34 +/- 0.04 mmol/l; p < 0.001) and higher levels of I- (11.5 +/- 5.7 vs. 3.0 +/- 1.9 pmol/l, p < 0.001) and C-iPTH (52 +/- 20.9 vs. 22.8 +/- 10.5 pmol/l; p < 0.001) than awakened dogs. Their stimulated (S) and nonsuppressible (NS) I-iPTH levels were increased 2- and 4-fold, respectively, while similar C-iPTH levels rose only 1.35- and 1.75-fold; this caused their S (4.4 +/- 0.7 vs. 6.8 +/- 1.9; p < 0.001) and NS (24.6 +/- 11.8 vs. 49.8 +/- 27.5; p < 0.05) C-iPTH/I-iPTH ratios to decrease. This was not explained by different renal clearance rates of I- and C-iPTH since both were similar at approximately 10 ml/kg/minute and unaffected by Ca2+ concentration. Clearance of all I- and C-iPTH HPLC molecular forms by the kidney appeared equal. A 50% decrease in the hepatic clearance of I-iPTH to approximately 12 ml/kg/minute in pentobarbital-anesthetized dogs, related to a lower hepatic blood flow, explained the higher levels of S and NS I-iPTH in these animals. I-iPTH hepatic clearance was unaffected by Ca2+ concentration. C-iPTH hepatic clearance was much lower at approximately 5 ml/kg/minute, abolished by hypercalcemia, and reduced by the influence of anesthesia on hepatic blood flow. This also explained the higher S C-iPTH levels in anesthetized animals. I-PTH(1-84) detected by the C-iPTH assay explained only 37.6% of the hepatic C-iPTH clearance in hypocalcemia and 73.3% in hypercalcemia. Overall, our results indicate that total C-iPTH clearance is about 40.2% that of I-iPTH in hypocalcemia and 41.3% in hypercalcemia. This would only explain a 2.4- to 2.5-fold difference in circulating levels of I- and C-iPTH if secretion rates were equal; the larger difference observed in S and NS C-iPTH/I-iPTH ratio values is thus mainly explained by different production rates.

Adjuvants, Anesthesia↗
PubMed1995

Differential toxicity of cisplatin, carboplatin, and CI-973 correlates with cellular platinum levels in rat renal cortical slices.

The differential toxicity of the platinum-containing compounds, cisplatin, carboplatin, CI-973, and transplatin, was investigated in renal cortical slices over a 24-hr period. Platinum accumulation was measured to assess whether platinum levels correlated with inhibition of specific cell functions (accumulation of organic ions, protein synthesis) or potassium loss. The earliest indicator of toxicity was decreased accumulation of the organic anion, para-aminohippuric acid (PAH), which preceded a decrease in the accumulation of the organic cation, tetraethyl-ammonium (TEA), and protein synthesis. Cisplatin (1 mM) and CI-973 (3 mM) treatment reduced PAH accumulation within 2 hr; carboplatin (3 mM) decreased PAH at 6 hr. TEA accumulation was absent in slices incubated for 6 hr or longer in 1 mM cisplatin, or for 24 hr in 3 mM carboplatin or CI-973. Protein synthesis was inhibited 80, 75, and 87% in slices treated for 24 hr with 100 microM cisplatin, 1 mM carboplatin, and 1 mM CI-973, respectively, compared to control. Intracellular potassium levels, which decreased between 6 and 24 hr, were the least sensitive indicator of cell damage. Transplatin, which lacks antitumor activity and is nonnephrotoxic in vivo, effectively decreased protein synthesis, intracellular potassium, and organic ion accumulation in rat renal cortical slices in vitro. The concentration of slice-associated platinum following treatment with cisplatin, carboplatin, CI-973, and transplatin increased with time and concentration. Inhibition of protein synthesis and loss of intracellular potassium correlated with increased total cellular platinum, indicating that platinum compounds negatively affect cell function and viability. The relative toxicity of these compounds in rat renal cortical slices was cisplatin = transplatin > CI-973 > carboplatin.

Animals↗
PubMed1994

Characterization of trihalomethane (THM)-induced renal dysfunction in the rat. II: Relative potency of THMs in promoting renal dysfunction.

Single non-lethal doses (3 mmol/kg) of chloroform (CHCl3), dichlorobromomethane (CHCl2Br), dibromochloromethane (CHClBr2), and bromoform (CHBr3) were administered by intraperitoneal injection to male Sprague-Dawley rats and proximal tubular secretion and reabsorption was assessed at varied times following treatment. Each of the trihalomethanes (THMs) at this dose inhibited proximal tubular secretion, as indicated by decreased in vitro renal cortical slice accumulation of organic anion p-aminohippuric acid (14C PAH). The time of maximal THM interference with 14C PAH uptake occurred at 8 h, with recovery being demonstrated by 48 h. Each of the THMs also demonstrated interference with tubular reabsorption, as assessed by urinary glucose excretion, with maximal interference occurring during the first day post-treatment and recovery being observed during the second day post-treatment. In each case, CHCl2Br was the most potent inhibitor of proximal tubular function. Combining these data with those of the preceding paper, the relative potency in disrupting renal function was, in general, CHCl2Br > CHCl3 > CHClBr2 > CHBR3. Since the time course of this investigation indicates that proximal tubular dysfunction precedes other THM-induced renal function interferences, it also appears that proximal tubular damage is the primary event leading to further manifestations of renal dysfunction.

Animals↗
PubMed1982

New formulas for the calculation of effective renal plasma flow.

Estimation of effective renal plasma flow (ERPF) can be made easily, inexpensively, and accurately by means of a single plasma concentration determination, sampled 44 min after injection of 131I-orthoiodohippurate (OIH). We originally established predictive regression equations based on a series of patients with a wide variety of diseases and a few normal potential kidney donors. The equation best fitting that data was parabolic in form and assumed a negative slope when high ERPF rates were encountered. This problem has been corrected by deriving new equations (parabolic and exponential) based on an expanded series which includes a large number of subjects with high ERPF. Errors of estimation are lower than those of the more classic para-aminohippuric acid (PAH) clearances and well within the exigencies of clinical practice.

Adolescent↗
PubMed1996

Changes in renal blood flow measured by radionuclide angiography following exhausting exercise in humans.

We measured renal blood flow (RBF) repeatedly in six male volunteers following exhausting cycling exercise using radionuclide angiography (RA) with technetium 99 m phytate (99 mTc-phytate), which is a nondiffusible radio-active tracer for kidney imaging and which is taken up quickly by the liver after injection into the circulation. The relationships between changes in RBF and creatinine clearance (Ccr), urine volume (UV) and plasma hormone involved in the regulation of renal function were also investigated. A bolus of 99 mTc-phytate (92.5 MBq.ml-1) was injected into the brachial vein via a catheter, while each subject was maintained in a supine position with his back to a scinticamera, which was connected to a computer for data processing. The pool transit time (PTT) was calculated from the time-concentration flow curve in the left kidney following injection of the bolus. The PTT normalized by the PTT of the heart (PTTn: kidney PTT/heart PTT), and the change in the reciprocal of PTTn (1/PTTn) were used as indices of the change in RBF. The resting RBF was also measured simultaneously by both RA and the para-aminohippuric acid (PAH) clearance method (CPAH). Post-exercise RBF was measured only by RA within 60 s of exercise, then again within 30 and 60 min of exercise on different days, since RBF can be measured successively only three times even with the use of 99 mTc-phytate. The resting value of 1/PTTn was converted to the value of CPAH corrected for haematocrit, and post-exercise change of 1/PTTn (RBF) was represented as a change in the value of CPAH in order to express a definite numerical change, rather than a percentage change, from resting RBF. The RBF decreased by 53.4% immediately after exercise, and remained decreased by 17.5% 30 min after and by 21.1% 60 min after exercise in comparison with the resting value. The RBF was found to be correlated with changes in Ccr (r = 0.773, P < 0.001), UV (r = 0.598, P < 0.001), and the concentrations of plasma angiotensin II (r = -0.686, P < 0.001) and noradrenaline (r = 0.652, P < 0.001) after exercise. However, there were no significant correlations between the changes in plasma aldosterone ([Ald]) and plasma noradrenaline, or in [Ald]p1 and plasma angiotensin II concentrations. The change in [Ald]p1 did not coincide with the variation in reabsorption of Na+ in the renal tubules. Results of the present study showed that change in Ccr after exhausting exercise depended mainly on change in RBF and that changes in UV and osmolality after exhausting exercise were induced not only by change in RBF, but also by changes in reabsorption of water and solutes in the renal tubules. It is suggested that changes in reabsorption of water and solutes might be influenced by metabolites induced by exercise and an increased release of hormones, other than aldosterone, involved in the regulation of renal function.

Adult↗
PubMed1986

Acute renal failure in children: prognostic features after treatment with acute dialysis.

A 12-year review (1972-1983) is presented of 76 children who were dialysed because of acute renal failure. The causes of acute renal failure were mainly the haemolytic-uraemic syndrome (53%), trauma (16%) and operation (13%). Fifty-eight children (76%) survived, 18 children (24%) died. Fifty-two children, the majority suffering from haemolytic-uraemic syndrome, regained complete or partial renal function after a period of dialysis lasting between 1 and 57 days. One to 7.7 years after dialysis, clearance studies with inulin (CIn), p-aminohippuric acid (CPAH) and phosphate (Tp/CIn) for staging renal function were carried out. The results of this investigation show a significant inverse correlation between the glomerular function regained and the duration of intermittent dialysis.

Acute Kidney Injury↗
PubMed1991

Angiotensin converting enzyme inhibitors for reduction of proteinuria in children with steroid-resistant nephrotic syndrome.

The effects of angiotensin converting enzyme inhibitors (ACEI) on proteinuria, renal function, and serum proteins were evaluated in six children with steroid-resistant nephrotic syndrome and proteinuria of 3-15 g/24 h (277 +/- 47 mg/m2 per hour). Following ACEI, proteinuria decreased from 7,408 +/- 2,385 (mean +/- SEM) to 3,746 +/- 1,395 mg/24 h (P less than 0.05). Creatinine clearance was 87.8 +/- 22.6 before and 96.4 +/- 23.6 ml/min per 1.73 m2 after ACEI. In two patients, inulin and para-aminohippuric acid clearances were normal before and after ACEI, together with parallel reductions of urine protein of 50% and 46%. Clearance of total protein was reduced by 56% following ACEI, compared with reduction in the clearance of gamma globulin by 58% and albumin by 39.5%. No significant change was seen in blood pressure, serum albumin, or total protein following ACEI. After ACEI, diuretic doses were able to be reduced or eliminated in three patients. Reduction of proteinuria was sustained during a followup period of 11-20 months in three patients. ACEI may be of benefit in the clinical management of children with steroid-resistant nephrotic syndromes, allowing reduction in diuretic requirements.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Renal function following unilateral nephrectomy for neuroblastoma and Wilms' tumour.

To estimate the side effects of chemotherapy and the influence of age at the time of nephrectomy on renal function, we investigated renal function in 34 uninephrectomised children with neuroblastoma (NB) or Wilms' tumour (WT). The results were compared with 6 controls who underwent nephrectomy for non-malignant disease. Study of renal function was primarily based on the clearance of inulin and para-aminohippuric acid (Cin and CPAH, ml/min per 1.73 m2). No significant differences in Cin/CPAH (mean +/- SD) were found between the NB group (90 +/- 24/421 +/- 95), WT group (85 +/- 17/386 +/- 104) and the controls (93 +/- 13/430 +/- 61). Children with NB and WT were divided into two subgroups according to the theoretical nephrotoxic risk. There was no significant difference in renal function between NB or between WT subgroups. Cumulative cisplatin doses in children with NB did not affect renal function significantly. The age at time of unilateral nephrectomy (< or = 2 years vs. > 2 years) was not associated with a higher risk of renal damage in WT children, whereas in NB children the filtration fraction (Cin:CPAH) was higher in younger children (mean +/- SD: 0.243 +/- 0.023 vs. 0.191 +/- 0.041). In conclusion, uninephrectomised children with NB are supposed to have a higher risk of drug-induced renal impairment compared with those with WT. Our data do not confirm this hypothesis, since renal function was comparable to controls in both groups, except in younger patients with NB who show a high filtration fraction. Since the survival of children with NB has improved, a longer follow-up of their renal function in needed.

Age Factors↗
PubMed1994

Glomerular volume and renal function in children with different types of the nephrotic syndrome.

Glomerular hypertrophy has been suggested to be an important factor in the pathogenesis of focal glomerular sclerosis. The aim of the present study was to analyse retrospectively the renal biopsies of 58 children (0.2-16.1 years of age) with different types of the nephrotic syndrome, minimal change nephrotic syndrome (MCNS), diffuse mesangial proliferation (DMP) and focal segmental glomerulosclerosis (FSGS). Glomerular surface area was measured and glomerular volume was calculated and related to steroid responsiveness and to renal function, measured by clearances of inulin and para-aminohippuric acid. Glomerular volume correlated with body surface area (BSA) and age. Because of this, patients with FSGS and DMP were matched according to BSA and age, with corresponding MCNS patients. Glomerular volumes of FSGS and DMP patients were significantly larger than those of MCNS patients. In the MCNS patients, significant correlations were found between glomerular volumes and glomerular filtration rate and effective renal plasma flow. Steroid-dependent and steroid-resistant patients showed larger glomeruli than the steroid-responsive children. We suggest that hyperfiltration and hyperperfusion, among other factors, may contribute to glomerular hypertrophy, mesangial proliferation and glomerulosclerosis.

Adolescent↗
PubMed1991

Urinary protein excretion and renal function in children with IgA nephropathy.

Renal haemodynamics and the pattern of urinary protein excretion were studied in 38 children (21 boys, 17 girls) with biopsy-proven IgA nephropathy (IgAN), 0.4-16.8 (median 5.3) years after onset of the disease. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were evaluated by clearances of inulin and para-aminohippuric acid. Serum and urinary albumin, IgG and beta 2-microglobulin (beta 2 mu) were determined and the excretion rates, clearances, and fractional clearances were calculated. The patients were grouped according to the type and the amount of proteinuria. Mean GFR and ERPF were significantly decreased (107 +/- 3 and 580 +/- 17 ml/min per 1.73 m2, respectively) versus controls (119 +/- 2 and 627 +/- 14 ml/min per 1.73 m2, respectively). Grouped according to albumin excretion rates, non-albuminuric patients had normal GFR, while mean GFR was reduced in patients with micro-albuminuria (106 +/- 3 ml/min per 1.73 m2) and albuminuric patients (92 +/- 7 ml/min per 1.73 m2). IgG excretion increased with increasing albuminuria, but the selectivity index was lower in albuminuric patients than in patients with micro-albuminuria. Albuminuric patients had also higher blood pressure than those with micro-albuminuria. beta 2 mu excretion did not discriminate between patients with impaired renal function. The results suggest that childhood IgAN is not a benign kidney disease. After a median duration of 5 years of the disease a number of children had impaired renal function. Mean GFR was reduced most in the albuminuric patients but was also decreased in micro-albuminuric patients, indicating that micro-albuminuria may be a predictor of more severe disease.

Adolescent↗
PubMed1995

Glomerular and tubular function in glycogen storage disease.

Urinary protein and calcium excretion were assessed in 77 patients with the hepatic glycogen storage diseases (GSD): 30 with GSD-I (median age 12.4 years, range 3.2-32.9 years), 25 with GSD-III (median age 10.5 years, range 4.2-31.3 years) and 22 with GSD-IX (median age 11.8 years, range 1.2-35.4 years). Inulin (Cinulin) and para-aminohippuric acid (CPAH) clearances were also measured in 33 of these patients. Those with GSD-I had significantly greater albumin (F = 15.07, P < 0.001), retinol-binding protein (RBP) (F = 14.66, P < 0.001), N-acetyl-beta-D-glucosaminidase (NAG) (F = 9.41, P < 0.001) and calcium (F = 7.41, P = 0.001) excretion than those with GSD-III and GSD-IX. GSD-I patients (n = 18) also had significantly higher Cinulin (F = 5.57, P = 0.009), but CPAH did not differ (F = 0.77, NS). Renal function was normal in GSD-III and GSD-IX patients. In GSD-I, Cinulin (r = -0.51, P = 0.03) and NAG excretion (r = -0.40, P = 0.03) were inversely correlated with age, whereas albumin excretion was positively correlated with age (r = +0.41, P = 0.03). RBP and calcium excretion were generally high throughout all age groups. Hyperfiltration in GSD-I is associated with renal tubular proteinuria that occurs before the onset of significant albuminuria. Deficiency of glucose-6-phosphatase within the proximal renal tubule may primarily cause tubular dysfunction, glomerular hyperfiltration being a secondary phenomenon.

Adolescent↗