Download the Free Unbound MEDLINE PubMed App to your smartphone or tablet.
Available for iPhone, iPad, iPod touch, and Android.
Renal AND Proteinuria [keywords]
- Prevalence of Microalbuminuria among Rural North Indian Population with Diabetes Mellitus and its Correlation with Glycosylated Haemoglobin and Smoking. [Journal Article]
- J Clin Diagn Res 2014 Jul; 8(7):CC11-3.
Macrovascular and microvascular complications of diabetes mellitus are a consequence of metabolic derangement mainly hyperglycemia. Diabetic nephropathy being one of them causes end stage renal disease. Hence, to detect renal involvement, microalbuminuria can be considered as an early marker.To study mean albumin creatinine ratio (ACR) in type 1 and type 2 diabetes mellitus with respect to HbA1c, duration of diabetes and smoking.Two hundred cases of type 1 and type 2 diabetes mellitus and 100 controls, age and sex matched were included in this study and measured for spot urinary albumin, spot urinary creatinine, fasting plasma glucose and HbA1c.It was observed that mean ACR was significantly elevated in type 1 and type 2 diabetes mellitus as compared to the controls. Mean ACR increases in diabetics with poor glycemic control, duration of diabetes and smoking.The early detection of microalbumin in diabetics can significantly reduce the progression of renal complications and before the development of proteinuria.
- Pharmacological manipulation of arachidonic acid-epoxygenase results in divergent effects on renal damage. [Journal Article]
- Front Pharmacol 2014.:187.
Kidney damage is markedly accelerated by high-salt (HS) intake in stroke-prone spontaneously hypertensive rats (SHRSP). Epoxyeicosatrienoic acids (EETs) are epoxygenase products of arachidonic acid which possess vasodepressor, natriuretic, and anti-inflammatory activities. We examined whether up-regulation (clofibrate) or inhibition [N-methylsulfonyl-6-(2-propargyloxyphenyl)hexanamide (MS-PPOH)] of epoxygenase would alter systolic blood pressure (SBP) and/or renal pathology in SHRSP on HS intake (1% NaCl drinking solution). Three weeks of treatment with clofibrate induced renal cortical protein expression of CYP2C23 and increased urinary excretion of EETs compared with vehicle-treated SHRSP. SBP and urinary protein excretion (UPE) were significantly lowered with clofibrate treatment. Kidneys from vehicle-treated SHRSP, which were on HS intake for 3 weeks, demonstrated focal lesions of vascular fibrinoid degeneration, which were markedly attenuated with clofibrate treatment. In contrast, 2 weeks of treatment with the selective epoxygenase inhibitor, MS-PPOH, increased UPE without significantly altering neither urinary EET levels nor SBP. Kidneys from vehicle-treated SHRSP, which were on HS intake for 11 days, demonstrated occasional mild damage whereas kidneys from MS-PPOH-treated rats exhibited widespread malignant nephrosclerosis. These results suggest that pharmacological manipulation of epoxygenase results in divergent effects on renal damage and that interventions to increase EET levels may provide therapeutic strategies for treating salt-sensitive hypertension and renal damage.
- [Effects of prednisone on renal FAK and Pyk2 expressions in rats with adriamycin- induced nephritis.] [JOURNAL ARTICLE]
- Nan Fang Yi Ke Da Xue Xue Bao 2014 Aug 20; 34(8):1149-1153.
To investigate the effects of prednisone on the expressions of FAK and Pyk2 in the kidneys of rats with adriamycin-induced nephritis.Thirty SD rats were randomized into normal control group, adriamycin-induced nephritic model group, and prednisone treatment group (n=10). Prednisone was administered at 10 mg/kg once daily in nephritic rats starting since the 7th day after adriamycin injection. Twenty-four-hour proteinuria was measured in the rats at different time points, and renal tissue histology was examined using transmission electron microscope. The expression levels of Pyk2, FAK and nephrin mRNA in the renal tissue were detected tested by RT-PCR, and the protein expressions of FAK, Pyk2, phosphorylated Pyk2 and phosphorylated FAK-Tyr397 were detected by Western blotting; immunohistochemistry was used for detecting nephrin protein expression in the kidney.Compared with the normal control group, the rats with adriamycin-induced nephritis showed significantly increased proteinuria (P<0.01), which was obviously lowered by prednisone treatment (P<0.01). Transmission electron microscopy revealed extensive fusion of the foot processes of the podocytes in the model group. Prednisone treatment promoted nephrin expression in the kidney (P<0.05). Compared with the control group, the model and prednisone treated groups showed significantly lowered nephrin mRNA expression (P<0.01) but increased FAK mRNA expression (P<0.01), but prednisone-treated group had a higher nephrin mRNA expression than the model group (P<0.05). The model group exhibited significantly increased expressions of FAK total and phosphorylated proteins, P-FAK/FAK, and P-Pyk2/Pyk2 (P<0.01), which were all lowered in the treatment group (P<0.01). Correlation analysis suggested that the expressions of FAK mRNA, FAK, pFAK, Pyk2 mRNA and pPyk2/Pyk2 were positively correlated with proteinuria (r=0.819, 0.750, 0.838, 0.762, 0.934, respectively, P<0.01).Adriamycin increases phosphorylated FAK and Pyk2 expressions to mediate kidney injury in rats. Prednisone inhibits Pyk2 and FAK activation, decreases proteinuria, and alleviates podocyte lesions to protect the glomerular filtration barrier.
- De novo amyloidosis in a renal transplant patient. [JOURNAL ARTICLE]
- Pediatr Transplant 2014 Sep 1.
Systemic AA amyloidosis is a serious complication of many chronic inflammatory disorders and chronic infections. Renal involvement is seen in the majority of the patients and can lead to end-stage renal disease. Renal transplantation can be performed in these patients; however, amyloidosis can recur in the transplanted kidneys. On the other hand, de novo AA amyloidosis in renal transplant patients has been rarely reported. We report a 17-yr-old patient with end-stage renal disease due to genitourinary anomalies who developed recurrent pyelonephritis after transplantation. Three yr after transplantation, renal biopsy was performed for proteinuria and AA amyloidosis was identified in the renal allograft. Although rare, chronic infections might cause de novo amyloidosis in renal transplant patients. Therefore, amyloidosis should be kept in mind in those types of patients who present with proteinuria.
- Dramatic effects of eculizumab in a child with diffuse proliferative lupus nephritis resistant to conventional therapy. [JOURNAL ARTICLE]
- Pediatr Nephrol 2014 Aug 31.
Treatment of systemic lupus erythematosus (SLE) with severe diffuse proliferative nephritis is often challenging, particularly in small children in whom a genetic conditioning is likely to play a role. The effectiveness of standard therapy based on glucocorticoid and immunosuppressive drugs is often unsatisfactory.A 4 year-old girl, whose parents were first-grade cousins of Moroccan ancestry, developed SLE that progressed to severe renal involvement despite standard therapy. She had persistently undetectable serum C4 levels and very low C3 levels (<30 mg/dl), and extremely high anti-DNA titers (>1:640) that remained unmodified during 2 years of follow-up. No mutations of genes encoding for complement inhibitors were detected. Despite aggressive therapy based on prednisone, plasma exchanges, and cyclosporine, the child worsened and eventually developed features of atypical hemolytic uremic syndrome (aHUS). Treatment with eculizumab provided prompt remission of vasculitis, proteinuria, and hematuria, with normalization of renal function. Two attempts to withdraw eculizumab were followed by severe relapses and rescued by reinstating treatment. The child has been treated with eculizumab for > 17 months without relevant side effects.C5 inhibition by eculizumab completely reversed clinical symptoms and laboratory renal signs of severe lupus nephritis. Blocking complement-system activation with the use of targeted drugs may be a new and exciting strategy to treat SLE patients unresponsive to conventional therapy.
- Early effect of NTBC on renal tubular dysfunction in hereditary tyrosinemia type 1. [JOURNAL ARTICLE]
- Mol Genet Metab 2014 Aug 1.
Hereditary tyrosinemia type 1 (HT1) is characterized by severe progressive liver disease and renal tubular dysfunction. NTBC therapy has revolutionized the management of HT1 but its effect on renal tubular function has so far been poorly investigated. The aim of this study was to describe the early effect of NTBC on renal tubular disease in patients with HT1.Five HT1 patients (age between 5 and 53months) with different types of presentation were evaluated before and during the first 2weeks of therapy with NTBC in a retrospective case analysis for phosphate metabolism and renal tubular function.Before starting NTBC therapy, all children manifested signs of renal dysfunction which included hypophosphatemia, acidosis, reduced phosphate reabsorption, aminoaciduria, glycosuria (Fanconi syndrome), and variable degree of proteinuria. Some patients also presented increased urinary calcium/creatinine ratio and raised fractional excretion of sodium. Starting of NTBC therapy resulted in the rapid normalization of plasma phosphate within one week from its initiation in majority of patients and in all patients during the second week of therapy. TmP/GFR normalized in 48h, while the other markers of renal dysfunction showed an improving trend over 2weeks.NTBC is an efficient treatment for renal tubular dysfunction in HT1, allowing the return to normal function within a few weeks. Its early effect on renal tubular cells appeared to be very rapid, particularly in normalizing plasma phosphate and TmP/GFR. In our series of patients, the TmP/GFR resulted as the most reliable index of tubular function.
- Consensus document for the detection and management of chronic kidney disease. [JOURNAL ARTICLE]
- Endocrinol Nutr 2014 Aug 26.
Chronic kidney disease (CKD) is an important global health problem, involving to 10% of the Spanish population, promoting high morbidity and mortality for the patient and an elevate consumption of the total health resources for the National Health System. This is a summary of an executive consensus document of ten scientific societies involved in the care of the renal patient, that actualizes the consensus document published in 2007. The central extended document can be consulted in the web page of each society. The aspects included in the document are: Concept, epidemiology and risk factors for CKD. Diagnostic criteria, evaluation and stages of CKD, albuminuria and glomerular filtration rate estimation. Progression factors for renal damage. Patient remission criteria. Follow-up and objectives of each speciality control. Nephrotoxicity prevention. Cardio-vascular damage detection. Diet, life-style and treatment attitudes: hypertension, dyslipidaemia, hyperglycemia, smoking, obesity, hyperuricemia, anemia, mineral and bone disorders. Multidisciplinary management for Primary Care, other specialities and Nephrology. Integrated management of CKD patient in haemodialysis, peritoneal dialysis and renal transplant patients. Management of the uremic patient in palliative care. We hope that this document may be of help for the multidisciplinary management of CKD patients by summarizing the most updated recommendations.
- Urinary messenger RNA of the receptor activator of NF-kappaB could be used to differentiate between minimal change disease and membranous nephropathy. [JOURNAL ARTICLE]
- Biomarkers 2014 Aug 29.:1-7.
Abstract Podocyte damage and loss together have an important role in the pathogenesis and progression of glomerulonephritis. Glomerulonephritis patients and healthy controls were enrolled in this study. Biochemical, clinical and experimental procedures included measurement of total urinary protein, renal biopsy and gene expression analysis of the receptor activator of NF-kappaB (RANK). The urinary mRNA levels of RANK were significantly higher in the glomerulonephritis group compared to the controls. The urinary RANK level of glomerular subtypes was correlated significantly with proteinuria. The calculated area of RANK mRNA levels under the curve was 0.61 for minimal change disease (MCD), 0.97 for membranous nephropathy (MN), 0.65 for IgA nephropathy (IgAN), 0.70 for lupus nephritis (LN) and 0.70 for focal segmental glomerulosclerosis (FSGS). The urinary mRNA of RANK might be used to differentiate histologic subtypes of glomerulonephritis, particularly between MCD and MN.
- Blocking Ligand Occupancy of the αVβ3 Integrin Inhibits the Development of Nephropathy in Diabetic Pigs. [JOURNAL ARTICLE]
- Endocrinology 2014 Aug 29.:en20141318.
Hyperglycemia stimulates secretion of αVβ3 ligands from vascular cells including endothelial cells resulting in activation of the αVβ3 integrin. This study determined if blocking ligand occupancy of αVβ3 would inhibit the development of diabetic nephropathy. Ten diabetic pigs received an F(ab)2 fragment of an antibody directed against the extracellular domain of the β3 subunit and ten received a control IgG F(ab)2 for 18 weeks. Non-diabetic pigs excreted 115 ± 50 μg of protein/mg creatinine compared to control F(ab)2 treated diabetic animals (218± 57 μg/mg) whereas diabetic animals treated with the anti-β3 F(ab)2 excreted 119 ± 55 μg/mg (p<0.05). Mesangial volume/glomerular volume increased to 21 ± 2.4 in control treated diabetic animals compared to 14 ± 2.8% (p<0.01) in animals treated with active antibody. Diabetic animals treated with control F(ab)2 had significantly less glomerular podocin staining compared to nondiabetic animals and this decrease was attenuated by treatment with anti-β3 F(ab)2. Glomerular basement membrane thickness was increased in the control, F(ab)2 treated diabetic animals (212±14 nm) compared to nondiabetic animals (170 ± 8.8 nm) but it was unchanged (159.9 ± 16.4 nm) in animals receiving anti-β3 F(ab)2. Podocyte foot process width was greater in control, F(ab)2 treated, animals (502± 34 nm) compared to animals treated with the anti-β3 F(ab)2 (357±47 nm, p<0.05). Renal β3 tyrosine phosphorylation decreased from 13,934 ± 6437 to 6730 ± 1524 (p<0.01) scanning units in the anti-β3 treated group. We conclude that administration of an antibody that inhibits activation of the β3 subunit of αVβ3 that is induced by hyperglycemia attenuates proteinuria and early histologic changes of diabetic nephropathy suggesting that it may have utility in preventing the progression of this disease complication.
- Inhibition of Hyperhomocysteinemia-Induced Inflammasome Activation and Glomerular Sclerosis by NLRP3 Gene Deletion. [JOURNAL ARTICLE]
- Cell Physiol Biochem 2014 Aug 20; 34(3):829-841.
Background/Aims: Hyperhomocysteinemia (hHcys) has been reported to initiate Nod-like receptor protein 3 (NLRP3) inflammasome formation and activation in podocytes, leading to glomerular dysfunction and sclerosis. However, it remains unknown whether Nlrp3 gene is critical for the formation and activation of inflammasomes in glomeruli of hHcys mice. Methods: Plasma homocysteine concentration was estimated utilizing HPLC, inflammasome formation and immunofluorescence expression from confocal microscopy, IL-1β production from ELISA. Results: Uninephrectomized Nlrp3 knockout (Nlrp3(-/-)) and wild type (Nlrp3(+/+)) and intra renal Nlrp3 shRNA-transfected wild type mice (Nlrp3 shRNA) were fed a folate free (FF) diet or normal chow (ND) for 4 weeks to produce hHcys. The plasma Hcys levels were significantly elevated in both Nlrp3(-/-) and Nlrp3(+/+) mice fed a FF diet compared to ND fed mice. The FF diet significantly increased the colocalization of Nlrp3 with apoptosis-associated speck-like protein (ASC) or caspase-1, caspase-1 activity and IL-1β production in glomeruli of Nlrp3(+/+), but not in Nlrp3(-/-) mice and local Nlrp3 shRNA transfected mice. Correspondingly, the glomerular damage index (GDI) and urinary protein excretion were significantly higher in Nlrp3(+/+) mice compared to ND fed mice. However, the hHcys-induced increase in GDI and proteinuria were significantly lower in Nlrp3(-/-) and local Nlrp3 shRNA transfected mice than in Nlrp3(+/+) mice. Immunocytochemical analysis showed that hHcys decreased expression of podocin and nephrin, but increased desmin expression in glomeruli of Nlrp3(+/+) mice compared to Nlrp3(-/-) mice. Conclusion: Nlrp3 gene is an essential component of Nlrp3 inflammasomes and that targeting Nlrp3 may be important therapeutic strategy to prevent inflammasome activation and thereby protect podocytes and glomeruli from hHcys-induced injury. © 2014 S. Karger AG, Basel.