Home About us Contact
|
Home About us Contact | ||
|
|
||
Tubular Dysfunction (tubular + dysfunction)
Selected AbstractsElectrophoretic analysis of urinary proteins in diabetic adolescentsJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 4 2001George Koliakos Abstract Pathological changes in the urine sodium dodecyl sulphate gel electrophoresis (SDS PAGE) patterns often precede the occurrence of any sign of renal involvement in diabetes. However, data concerning the most frequent SDS PAGE pattern of the urine in early stages of type I diabetes mellitus are controversial. In the present study an SDS PAGE technique has been used that provides an adequate sensitivity for the detection of the abnormal pattern. Urinary proteins have been analyzed by SDS PAGE in twenty two diabetic adolescents and twenty four age matched controls. Albumin concentration, and N acetyl-beta-D-glucosaminidase (NAG) activity were also measured in the same samples. There was no significant difference in urine albumin concentration and NAG activity between diabetic children and controls. However twelve patients showed an electrophoretic pattern characteristic for glomerulopathy, two had a pattern indicating tubular dysfunction and another two patients had a mixed pattern. Among the twenty four controls only three showed abnormal electrophoretic patterns. The results support the view that early stages of diabetic nephropathy may involve both glomerular and tubular dysfunction. However the exact clinical and prognostic significance of the information provided by SDS PAGE analysis remains to be elucidated. J. Clin. Lab. Anal. 15:178,183, 2001. © 2001 Wiley-Liss, Inc. [source] Clinicopathology of childhood-onset renal systemic lupus erythematosusNEPHROLOGY, Issue 4 2007WASIU A OLOWU SUMMARY: Aims: To determine the clinicolaboratory renal manifestations; glomerular, extra-glomerular histopathologic lesions; renal tubular dysfunction (RTD) frequency and outcome of a short-term renal follow up in Nigerian children with systemic lupus erythematosus (SLE). Methods: A non-randomized prospective study of consecutive cases of childhood-onset SLE with nephropathy was conducted. Baseline/follow-up clinicolaboratory data were collected. Each patient was followed up for 12 months. Results: Seven of the 11 children studied were girls. The median age at diagnosis was 11.0 years. Median diagnosis time interval (1.9 years) and median time of renal disease onset (1.0 year) were similar. Hypertension, nephrotic syndrome and acute renal failure (ARF) occurred in 45.5%, 54.5% and 63.7% of the patients, respectively. The glomerular lesions were non-proliferative lupus nephritis (LN) in 9.0% (class II LN); focal (class III LN) and diffuse (class IV LN) proliferative LN (PLN) in 27.0% and 64.0%, respectively. Tubulointerstitial nephritis (TIN, 91.0%) and RTD (64.0%) were common. ARF (P = 0.033) and RTD (P = 0.015) were significantly associated with severe TIN. Complete renal remission rate at end-point was 71.4%. Relapse and renal survival rates were 14.3% and 86.0%, respectively. RTD was persistent in 43.0%. Conclusion: Renal function disorders, diffuse PLN and extra-glomerular lesions were frequent. Significant association of ARF and RTD with severe TIN in this series suggests the need for early renal tubular function (RTF) assessment in our SLE patients. Deranged RTF may be marker of severe TIN in SLE warranting early confirmatory renal biopsy and aggressive interventional treatment. [source] Renal tubular function in children with ,-thalassemia minorNEPHROLOGY, Issue 5 2005SÜLEYMAN KALMAN SUMMARY: Background: , -thalassemia minor is a common heterozygous haemoglobinopathy that is characterized by both microcytosis and hypochromia. It requires no treatment. It has been postulated that low-grade haemolysis, tubular iron deposition and toxins derived from erythrocytes might cause renal tubular damage in adult patients with , -thalassemia minor. Our aim was to investigate the renal tubular functions in children with ,-thalassemia minor and to determine its possible harmful effects. Methods: The study was conducted on 32 children (14 female and 18 male) at the age of 5.8 ± 3.1 years (range 2,14 years) with , -thalassemia minor. The patients were classified as anaemic (haemoglobin (Hb) , 11 g/dL) (Group 1, n = 14) and non-anaemic (Hb > 11 g/dL) (Group 2, n = 18). A control group was formed with 18 healthy children whose ages and sexes match those in other groups (Group 3, n = 18). Fractional excretion of sodium (FENa, %), fractional excretion of magnesium (FEMg, %), fractional excretion of uric acid (FEUA, %) and tubular phosphorus reabsorption (TPR,%) were calculated with standard formulas. Urinary calcium excretion (mg/kg per 24 h), zinc (Zn) (µg/dL), glucosuria (mg/dL), , -2 microglobulin (mg/dL) and N -acetyl- ,,D-glycosaminidase (NAG, U/mmol creatinine) levels were measured through biochemical methods. Results: There was no statistically significant difference among the three groups in terms of the results of FENa (%), FEMg (%), FEUA (%), TPR (%), calciuria (mg/kg per 24 h), NAG, urine Zn, proteinuria, glucosuria or urine , - 2 microglobulin levels (P > 0.05). Conclusion: On the contrary of children with , -thalassemia major, renal tubular dysfunction has not been determined in children with , -thalassemia minor in the present study. [source] Paraquat-induced Fanconi syndromeNEPHROLOGY, Issue 5 2005HYO W GIL SUMMARY: The ingestion of paraquat, a non-selective herbicide, can be fatal in humans. Paraquat is toxic to multiple organs, including the kidney, heart, gastrointestinal tract and central nervous system. Although paraquat has been established as one cause of acute tubular necrosis, Fanconi syndrome presenting as severe hypophosphataemia after paraquat intoxication has not been reported. Here, we report the case of a 44-year-old Korean woman who presented with generalized proximal tubular dysfunction including aminoaciduria, phosphaturia and glycosuria after paraquat intoxication. We found that severe hypophosphataemia induces deep drowsiness. Renal biopsy findings indicated the presence of acute tubular necrosis that may be reversible. [source] Fanconi's syndrome and subsequent progressive renal failure caused by a Chinese herb containing aristolochic acidNEPHROLOGY, Issue 3 2004SANGHO LEE SUMMARY: Chinese herb nephropathy contains a variety of clinical features of progressive renal failure (indicated by studies conducted in Belgium) to the variant type of Fanconi's syndrome. Fanconi's syndrome has mostly been reported in Asian countries, and is characterized by proximal tubular dysfunction and slower progression to end-stage renal disease (ESRD); it also often revealed a reversible clinical course. We describe a 43-year-old woman who presented with polyuria and polydipsia caused by Fanconi's syndrome. The cause of Fanconi's syndrome was not identified because the patient denied the intake of the Chinese herbal mixture at first. Fanconi's syndrome seemed to be reversible in its early stage, but it rapidly progressed to renal failure after 3 months, despite the interruption of Chinese mixture use. A renal biopsy revealed typical findings of aristolochic acid-induced nephropathy. Aristolochic acids were also detected in the Chinese herbs that were consumed. This case highlights the variety of the clinical spectrum of aristolochic acid induced nephropathy (AAN). We emphasize that AAN should be suspected in all patients with Fanconi's syndrome, even if patients deny the intake of any Chinese herbal preparation. [source] Renal Fanconi syndrome and myopathy after liver transplantation: Drug-related mitochondrial cytopathy?PEDIATRIC TRANSPLANTATION, Issue 1 2008Umut Selda Bayrakci Abstract:, Advances in the field of transplantation provide a better quality of life and allow more favorable conditions for growth and development in children. However, combinations of different therapeutic regimens require consideration of potential adverse reactions. We describe a 15-yr-old girl who had orthotopic liver transplantation because of Wilson's disease. Tacrolimus, MMF, and steroids were given as immunosuppressant. Lamivudine was added because of de nova hepatitis B infection during her follow-up. Three yr after transplantation she developed renal Fanconi syndrome with severe metabolic acidosis, hypophosphatemia, glycosuria, and aminoaciduria. Although tacrolimus was suspected to be the cause of late post-transplant renal acidosis and was replaced by sirolimus, acidosis, and electrolyte imbalance got worse. Proximal muscle weakness has developed during her follow-up. Fanconi syndrome, as well as myopathy, is well recognized in patients with mitochondrial disorders and caused by depletion of mtDNA. We suggest that our patient's tubular dysfunction and myopathy may have resulted from mitochondrial dysfunction which is triggered by tacrolimus and augmented by lamivudine. [source] Glomerular dysfunction, independent of tubular dysfunction, induced by antineoplastic chemotherapy in childrenPEDIATRICS INTERNATIONAL, Issue 5 2004Yukie Ikarashi AbstractBackground:,For the purpose of studying renal side-effects induced by antineoplastic agents, the authors examined glomerular injury as well as tubular injury of patients with chemotherapy. Methods:,Thirteen patients underwent a combined total of 64 courses of chemotherapy. Urinary albumin, ,2-microglobulin (,2-MG), N-acetyl-,-glucosaminidase (NAG) and urinary protein were measured before and serially after chemotherapy. Results:,The values of albumin/creatinine (albumin/cre) ratio and ,2-MG/creatinine (,2-MG/cre) ratio after chemotherapy were higher than those before chemotherapy (P < 0.01). NAG/creatinine (NAG/cre) ratio and creatinine clearance (Ccr) were not different. These were also examined before the next course of chemotherapy and were compared with those of control children. Albumin/cre ratio was significantly different (P < 0.01). ,2-MG/cre ratio and NAG/cre were not different. Furthermore, in patients with normal ,2-MG/cre, the albumin/cre ratio was significantly higher than in control children. Conclusions:,These results indicate that antineoplastic agents can not only induce tubular dysfunction but also glomerular dysfunction, which is persistent and independent of tubular dysfunction. [source] Effect of perioperative steroids on renal function after liver transplantation,ANAESTHESIA, Issue 3 2006S. Turner Summary Subclinical renal dysfunction is thought to occur as a systemic manifestation of ischaemia-reperfusion injury of other organs. Liver transplantation is associated with major ischaemia-reperfusion injury. Thirty-four patients undergoing elective liver transplantation were randomly allocated to receive either saline or 10 mg.kg,1 methylprednisolone on induction of anaesthesia. Urine was taken for N-acetyl-,-D-glucosaminidase, creatinine and other markers of tubular function. Serum chemistry was measured for 7 days. Creatinine concentration increased in the saline group but not in the methylprednisolone group (p < 0.0001), with the greatest difference on the third postoperative day (mean (SD) 164.8 (135.8) ,mol.l,1vs 88.5 (39.4) ,mol.l,1, respectively). Similar changes were seen in postoperative alanine transferase (865 (739) U.l,1vs 517 (608) U.l,1, respectively; p <,0.0001) on the second postoperative day. Both groups exhibited increases in markers of renal tubular dysfunction and of glomerular permeability. Patients in the saline group sustained more adverse events (8/17 (47%) vs 2/17 (12%); p = 0.02). The data confirm increased proximal tubular lysosomal turnover, consistent with an increased tubular protein load, following liver transplantation, and suggest that methylprednisolone protects against renal and hepatic dysfunction. [source] | ||||||||||