Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the morphological changes in renal proximal tubules at the onset of diabetic nephropathy, we observed 177 biopsy samples from patients with Non-Insulin-Dependent Diabetics (NIDDM) using light and electron microscopy. Group I had no proteinuria (p.u.), group II had p.u. < or = 0.5 g/day, group III had p.u. > 0.5 g/day, group IV had serum creatine level (Cr) > 1.5 mg/dl. Twenty age-matched normal patients and 80 patients with IgA nephropathy were used as controls. In groups I and II, the following features were significantly different from those in the controls: spherical enlargement of mitochondria (MT) in proximal tubule cells, hypertrophy of proximal tubule cells and their nuclei, and thickening of both the proximal tubule basement membrane (TBM) and the glomerular basement membrane (GBM). Among the histological changes observed in group I, the thickness of the GBM and TBM indicated that the disease would lead to diabetic nephropathy. MT enlargement was positively correlated with nuclear and cytoplasmic enlargement of the proximal tubule cells in diabetic patients (p < 0.05), but was not correlated with other morphological changes or disease prognosis. Glomerular nodular lesions, glomerular sclerotic change, and cortical tubulointerstitial fibrosis became evident in groups III and IV. From the above, we concluded that MT enlargement and thickening of the TBM are possible causes of reduced active transport in the proximal tubules, causing microalbuminuria in diabetics, and initial impairment of post-tubule transport.
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PMID:Mitochondrial enlargement and basement membrane thickening of renal proximal tubules, possible initiators of microalbuminuria in non-insulin-dependent diabetics (NIDDM). 147 27

The intrarenal hemodynamics was examined in 101 patients with chronic glomerulonephritis (CGN) and 111 patients with type I diabetes mellitus. Intrarenal hypertension was diagnosed from renal functional reserve (RFR) depletion. In CGN intrarenal hypertension was revealed in all clinical and morphological variants of nephritis: in 40% of patients with a nephrotic variant, in 25% with a latent variant and in 83% of patients with nephritis concurrent with the severe urinary syndrome. In focal segmental glomerulonephritis and fibroplastic nephritis, the depleted RFR was encountered 4 times more frequently than the preserved one. There was a association between RFR and arterial hypertension, albuminemia, blood creatinine. In diabetes mellitus intraglomerular hypertension was diagnosed in 34% of patients without renal damage (those having normal albuminuria), in 79% at the preclinical stage of diabetic nephropathy (in microalbuminuria) and in 93% at its clinical stage. Intrarenal hemodynamic disorders in diabetes mellitus are primary and provoked by hormonal metabolic disorders. The morphological signs of renal hyperperfusion failure develop at the preclinical stage of diabetic nephropathy.
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PMID:[Disorders of intrarenal hemodynamics in glomerulopathies]. 762 86

Renal haemodynamics and urinary protein excretion (UPE) were investigated in 36 patients with IgA nephropathy more than 3 years after renal biopsy (mean interval 6.3 +/- 0.5 years). At follow-up, 39% of patients had a reduced glomerular filtration rate (GFR) and 11% endstage renal failure. Twenty-five percent had albuminuria, and a further 25% microalbuminuria. All albuminuric patients had GFRs below the mean, and 78% of the albuminurics had a reduced GFR. However, non-albuminurics also had decreased GFRs and GFR tended to fall with the duration of the disease in this group of patients. On comparing the histological changes in the biopsies with haemodynamic and UPE studies performed 6 years later, we found significant correlations between the extent of segmental glomerular sclerosis and GFR, effective renal plasma flow, urinary albumin and IgG excretion, respectively. Histological grading correlated with the same variables. Of the 4 uraemic patients, 2 were nephrotic at presentation, while the other 2 had a nephritic onset of disease and later developed heavy proteinuria. Three of their biopsies showed > or = 10% segmental glomerulosclerosis. Juvenile IgA nephropathy is not a harmless disease. Our results indicate that these children should be carefully monitored with adequate GFR measurements and urine protein analyses.
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PMID:Follow-up of renal function and urinary protein excretion in childhood IgA nephropathy. 847 2

Urinary microalbumin excretion was assessed in 76 children with asymptomatic microscopic hematuria in whom the presence of proteinuria, hypertension, reduced renal function, hypercalciuria, urinary tract infection or structural abnormality of the urinary tract had been excluded. All children underwent a percutaneous kidney biopsy to determine whether microalbumin excretion can be used as a marker to predict the source of hematuria. Microalbumin excretion was considered normal if the urinary ratio of microalbumin to creatinine (MA/Cr ug/mg) was < or =30. Twenty-two (29%) had microalbuminuria (MA/Cr 96+/-30 microg/mg) and 54 (71%) had normal albumin excretion (MA/Cr 13+/-2 microg/mg). Of those with normoalbuminuria, 38 (70%) had normal renal tissue, 15 (28%) thin glomerular basement membrane (TGBM) disease and 1 (2%) IgA nephropathy. In contrast, 20 (91%) of those with microalbuminuria had IgA nephropathy and 2 (9%) had TGBM disease. The mean urinary MA/Cr ratio for all IgA children was 89+/-32 microg/mg higher compared with a value for the children with TGBM disease (14 +/-3 microg/mg, P <0.001) or children whose renal biopsy appeared normal (11+/-2 microg/mg, P <0.001). Statistical analysis revealed no significant differences between the mean MA/Cr ug/mg ratio for children with TGBM disease and those with normal glomerular findings. Fourteen of the 20 children with IgA nephropathy who also had microalbuminuria were treated with an angiotensin-converting enzyme (ACE) inhibitor. Over a mean follow-up of 51 months, none developed overt proteinuia; hematuria resolved and microalbuminuria returned to normal in eight (57%) during therapy with the ACE-inhibitor. In contrast, hematuria persisted and prtoteinuria developed in the other untreated children. None of the children with TGBM disease developed overt proteinuria after a mean of 51 months. Hematuria was persistent in children with TGBM disease, but often resolved in those whose biopsies were completely normal. These data suggest that determination of urinary microalbumin excretion is warranted in the routine examination of children with isolated microscopic hematuria. Routine screening for microalbuminuria may help to identify a subgroup of patients with IgA nephropathy who are at high risk for progressive kidney disease and need more intensive therapy and closer follow-up.
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PMID:Value of urinary excretion of microalbumin in predicting glomerular lesions in children with isolated microscopic hematuria. 1594 87

It has been suggested that the finding of acanthocyturia in patients with hematuria points to the presence of glomerulonephritis. However, little attention has been paid to the finding of acanthocyturia in diabetic patients with hematuria. Here we studied 93 consecutive diabetic patients and explored the prevalence of microscopic hematuria and acanthocyturia in association with normoalbuminuria (NO; urinary albumin excretion (UAE) of < 30 mg/g x creatinine), microalbuminuria (MI; UAE of 30-299mg/g x creatinine), macroalbuminuriaMA; UAE of > or = 300mg/g x creatinine), or chronic renal failure (CRF; serum creatinine levels of > or = 1.1mg/dl for male and > or = 0.9mg/dl for female). We defined microscopic hematuria as > or = 5 erythrocytes per high-power field and acanthocyturia as > or = 5% acanthocytes (erythrocytes of doughnut-like appearance with vesicle-shaped protrusions) among 100 erythrocytes in the centrifuged urinary sediment. Microscopic hematuria was found in 12 (24%) out of 49 patients with NO, in 9 (43%) out of 21 patients with MI, in 6 (75%) out of 8 patients with MA, and in 7 (47%) out of 15 patients with CRF. Patients with microscopic hematuria showed a significant increase in urinary albumin excretion as compared to those without (836 +/- 265 vs. 135 +/- 56, p < 0.01). Of patients with microscopic hematuria, acanthocyturia was observed only in 2 (22%) out of 9 patients with MI and in 2 (33%) out of 6 patients with MA. Two of 4 patients with acanthocyturia had elevated serum levels of IgA and chronic tonsillitis, which indicated the occurrence of IgA nephropathy in these patients. Thus, microscopic hematuria was common and associated with elevated UAE, while acanthocyturia was rare and observed only in patients with elevated UAE. We propose that more attention should be paid to the finding of acanthocyturia in diabetic patients with hematuria and albuminuria.
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PMID:[Hematuria and acanthocyturia in patients with diabetes]. 1637 48

There has been a major increase in obesity among children over the past twenty years. Obesity is associated with glomerular hyperperfusion and hyperfiltration from physiological (mal)adaptation resulting from afferent arteriolar vasodilatation. The renal injury from hyperfiltration in obesity is further exacerbated by concomitant presence of dyslipidemia, hyperglycemia and/or insulin resistance, inflammation and hypertension. The renal injury clinically manifests as microalbuminuria, proteinuria and/or poor renal function, and is histologically characterized by glomerulomegaly, mesangial expansion and/or sclerosis, which has been termed "obesity related glomerulopathy". Obesity portends a poor prognosis in subjects with chronic kidney diseases, IgA nephropathy and nephrectomy. Obese individuals on dialysis and renal transplant have mixed outcomes. The purpose of this review is to highlight the nondiabetic consequences of obesity on kidney for the pediatric nephrology community as we begin to address the obesity epidemic in children.
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PMID:Nondiabetic consequences of obesity on kidney. 1649 17

Among adult patients with isolated microscopic haematuria (IMH) which is defined as persistent microscopic haematuria but without proteinura, hypertension, renal insufficiency, urinary tract infection or structural abnormality of the urinary tract, some patients have chronic glomerulonephritis (CGN), in whom early diagnosis by renal biopsy is beneficial to timely intervention. Nevertheless, a considerable number of patients with optimistic prognosis [e.g. thin basement membrane nephropathy (TBMN)] undergo invasive and needless renal biopsy. Indicators for weighing the necessity of renal biopsy would be clinically significant. To investigate the value of urinary albumin/creatinine ratio (UACR), serum IgA level, serum C3 level and serum IgA to C3 ratio in predicting the necessity of renal biopsy for adult patients with IMH, 216 patients were studied retrospectively. Patients were divided into: (CGN group, n=137), (TBMN group, n=56) and normal biopsy (normal group, n=23). Of all patients, 131 (61%) evidenced microalbuminuria (UACR=30-299 mg/g) and 85 (39%) had normoalbuminuria (UACR<30 mg/g). The mean value of UACR in CGN group was higher (96+/-17 mg/g) compared with that in TBMN (20+/-4 mg/g, p<0.01) or normal (18+/-3 mg/g, p<0.01) group. The mean values of serum IgA and serum IgA/C3 ratio in patients with IgA nephropathy (IgAN) were significantly higher than those with non-IgAN (380+/-103:217+/-99 mg/dl, p<0.01; 4.5+/-1.2 : 2.4+/-0.9, p<0.01). The odds ratio for distinguishing IgAN from non-IgAN was significantly correlated with serum IgA level and serum IgA to C3 ratio. For adult patients with IMH, UACR, serum IgA level and serum IgA to C3 ratio are non-invasive markers for predicting the necessity of renal biopsy.
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PMID:Useful indicators for performing renal biopsy in adult patients with isolated microscopic haematuria. 1736 78

IgA nephropathy is currently the most frequently investigated glomerulonephritis. The disease is defined by the presence of dominant or co-dominant deposits of IgA1 in the glomerular mesangium. Circulating immune complexes are most likely the source of the deposited IgA1. However, it is also possible that the aggregates of structurally altered IgA1 or enhanced binding to IgA receptors expressed on mesangial cells lead to deposition. The cause of the formation of immune complexes responsible for IgA nephropathy lies in the incomplete O-linked oligosaccharide side chains, which, due to the deficiency of corresponding glycosyltransferases, lack terminal galactose residues leading to the exposure of N-acetylgalactosamine. Naturally occurring antibodies of the IgG or IgA1 isotype bind to this sugar antigen. In the clinical course, we differentiate between the early stage usually characterized by hematuria, and a variable late stage characterized either by a clinical remission, by persistence of hematuria, or by increasing proteinuria and blood pressure and decreasing renal function in one third of the patients. In the early stage, it is difficult to predict the prognosis of IgA nephropathy, either on the basis of clinical presentation and morphological findings, or according to the level of galactose-deficient IgA1 in the circulation. The reliable criteria of serious prognosis emerge only in the later stages of the disease and include proteinuria, hypertension, and histologically apparent tubular atrophy and interstitial sclerosis. The dominant trend in the treatment of IgA nephropathy is the emphasis on administration of ACE inhibitors/sartans, which are introduced into the treatment at the time of microalbuminuria. If proteinuria does not decrease below 1 g/24 h, treatment with prednisone is justifiable. New findings concerning the molecular/cellular mechanism involved in the pathogenesis of IgA nephropathy suggest the possible therapeutical interference with the generation of nephritogenic immune complexes by a selective blocking of the IgA1 molecules with altered glycan structures using monovalent reagents.
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PMID:[IgA Nephropathy. Facts, uncertainties, and potential causal therapy approaches]. 2635 58