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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A prospective multicenter study was designed to determine the frequency and prognostic importance of hypercalciuria in children with hematuria. Urinary calcium excretion was examined in 215 patients with unexplained isolated hematuria (no proteinuria, urolithiasis, infection or systemic disorder). Hypercalciuria (urinary calcium excretion greater than 4 mg/kg/day) was identified in 76 patients (35%). Compared to patients with normal urinary calcium excretion, children with hematuria and hypercalciuria were characterized by male preponderance, white race, family history of urolithiasis, gross hematuria and calcium oxalate crystals. Renal biopsies were performed in 10 patients with urinary calcium excretion 0.4 to 2.5 mg/kg/day; three had IgA glomerulonephritis, three had glomerular basement membrane thinning, one had proliferative glomerulonephritis and three were normal. Renal biopsies in three patients with hypercalciuria showed focal segmental glomerulosclerosis, hereditary nephritis or no abnormalities. Oral calcium loading tests showed renal hypercalciuria in 26 patients, absorptive hypercalciuria in 15 patients and were not diagnostic in 35 patients. Serum parathyroid hormone, bicarbonate and phosphorus and urinary cyclic adenosine monophosphate concentrations were similar in the three groups of hypercalciuric patients. Urinary calcium excretion after one week of dietary calcium restriction was higher (5.8 mg/kg/day) in renal hypercalciuria than in other hypercalciuric patients (3.4 mg/kg/day), P less than 0.01. One to four years follow-up was available for 184 patients. Eight of 60 hypercalciuric patients developed urolithiasis or renal colic compared to 2 of 124 patients with normal urinary calcium excretion (P less than 0.001). Hypercalciuria is commonly associated with isolated hematuria and represents a risk factor for future urolithiasis in children with hematuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Idiopathic hypercalciuria: association with isolated hematuria and risk for urolithiasis in children. The Southwest Pediatric Nephrology Study Group. 240 91

In their review the authors discuss the history of Alport's syndrome, its nomenclature, incidence, genetics, clinical diagnosis. The authors emphasize electron microscopic findings and criteria of the diagnosis (haematuria or renal failure in the family, progressive nervous deafness, typical changes of the basal glomerular membrane (GBM) and ophtalmological findings of lenticonus or perimacular spots. Familial haematuria (FH) is according to the authors defined as haematuria in several members of the family. Based on data in the literature and the authors' experience, the authors discuss the differential diagnosis of FH where Alport's syndrome is relatively rare. A far more frequent unit is benign familial haematuria characterized morphologically as isolated thinning of the GBM. In some cases these patients are threatened by iatrogenic damage from unnecessary and invasive diagnostic method. The finding of thinned GBM and normal renal function in the parents and grandparents suggest a favourable prognosis also in child patients. Cases of familial glomerulonephritis or idiopathic syndrome with glomerulosclerosis or familial IgA nephropathies are relatively rare. Familial haematuria is are relatively rare. Familial haematuria is relatively frequent (according to the authors 20% of all obscure haematurias) and their diagnosis is based on systematic examination of the urine in other members of the patient's family who also suffer from haematuria.
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PMID:[Familial hematuria and Alport's syndrome]. 265 95

Thin-basement-membrane nephropathy, also called benign recurrent hematuria, is characterized by diffuse thinning of the glomerular basement membrane and by hematuria. To determine the incidence of thin-basement-membrane nephropathy among patients with idiopathic hematuria, we conducted a prospective study in the nephrology units of three large hospitals in the Netherlands. Eighty normotensive adults without azotemia underwent renal biopsy because of recurrent macroscopic hematuria (n = 26) or persistent microscopic hematuria (n = 54). Idiopathic IgA nephropathy was found in 27 of the 80 patients. Light microscopical examination showed that 42 patients had normal renal tissue. The remaining 11 patients had mesangioproliferative glomerulonephritis (n = 5), interstitial nephritis (n = 3), or focal global glomerulosclerosis (n = 3). Tissue from the 42 patients whose renal biopsy specimens were normal when examined with light microscopy was analyzed morphometrically with electron microscopy to determine the thickness of the glomerular basement membrane. Two subsets of patients were identified by this analysis. In 18, thin-basement-membrane nephropathy was found (mean basement-membrane thickness [+/- SE], 191 +/- 28 nm; normal, 350 +/- 43 nm); all but one of these 18 patients had microscopic hematuria, which persisted during follow-up (median duration, 50 months). (Of the 54 patients who presented with microscopic hematuria, 17 [31 percent] had thin-basement-membrane nephropathy.) The thickness of the glomerular basement membrane was normal in the other 24 patients (361 +/- 69 nm); during follow-up, hematuria disappeared in all 13 of these patients who had macroscopic hematuria, and hematuria resolved in 5 of the 11 patients who had microscopic hematuria. We conclude that in patients with persistent microscopic hematuria, the incidence of thin-basement-membrane nephropathy is similar to that of idiopathic IgA nephropathy. Morphometric analysis of the thickness of the glomerular basement membrane should be included in the workup of adults with persistent microscopic hematuria that is not of urologic origin.
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PMID:Thin-basement-membrane nephropathy in adults with persistent hematuria. 290 74

Recently the appearance of deformed polymorphous erythrocytes in the urinary sediment has been described as characteristic of glomerular bleeding. We studied 30 patients with histologically confirmed glomerular disorders and 25 patients with urological diseases and with hematuria. In the sediment of 10 ml urine 200 erythrocytes were counted under phase-contrast microscopy and evaluated relative to their morphology. The number of glomerular erythrocytes was expressed as a percentage. In all groups of glomerular disorders (mesangial-proliferative, membranous and membrano-proliferative glomerulonephritis, focal segmental glomerulosclerosis, glomerulonephritis of systemic disease, thinning of the glomerular basement membrane) the percentage of glomerular erythrocytes varied widely between 2 and 100%. In 7 cases less than 10% of glomerular erythrocytes were found. There was no correlation between the percentage of glomerular erythrocytes and the degree of renal insufficiency, hematuria or proteinuria. On the other hand, in patients with hematuria from the lower urinary tract, erythrocytes were uniformly non-glomerular in shape (95-100%). We conclude that 10-20% or more of glomerular erythrocytes in the urinary sediment are a good indicator of glomerular disease, whereas lower figures do not definitely rule out a glomerular origin for hematuria.
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PMID:[Diagnosis of glomerular and non-glomerular erythrocyturia using phase contrast microscopy of the urine sediment]. 331 Feb 12

20 puncture renal biopsies and 16 pancreatic biopsies from patients with insulin-dependent diabetes mellitus were studied ultrastructurally. The stages in the development of kidney changes depending on the functional state of Langerhans islands B-cells were established. The 1st stage includes signs of segmentary mesangioproliferative glomerulonephritis- segmentary increase of the mesangium due to the hypercellularity, variability of the basal membrane thickness in the glomeruli capillaries, leucocytes in the lumen, subendothelial deposits. This stage may be due to the persistence of the etiologic factors(virus), formation of circulating immune complexes, antibodies excess and relative preservation of B-cells and their function. Thinning of the capillary basal membrane, decrease of the mesangial matrix surface, cell destruction are characteristic for the 2nd stage- stage of the mesangiolysis. The duration of disease up to 15 years has no influence on the formation of glomerulosclerosis.
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PMID:[Diabetic glomerulonephritis--the first stage of diabetic glomerulopathy]. 784 5

Hyperlipidemic rats, which have been described as a useful animal model for focal glomerulosclerosis in humans, were examined at the ages of 17, 20, 24, and 27 weeks for evaluation of spontaneously developed coronary arterial lesions. The mean concentrations of cholesterol, triglyceride, phospholipid, and urea nitrogen were greater than the respective control concentrations at and after the age of 17 weeks. No abnormalities were detected in the blood pressure values. Starting from the age of 24 weeks, the rats had disseminated white spots in the ventricles and septum of the heart. Mean renal weights of hyperlipidemic rats were higher than those of control rats at the ages of 17 and 20 weeks, and the surface of the kidney appeared irregular when rats were 27 weeks old. Histologic examination revealed atrophy of the coronary artery, a decrease in the number of smooth muscle cells, and thinning of the wall, resulting in loss of the normal wall structure. A homogenous eosinophilic substance, the nature and cause of which were unknown, was also seen in the affected arterial walls. Furthermore, white spots observed macroscopically were found to represent myocardial degeneration and necrosis with reactive histiocytic cells and lymphocytes, adventitial fibrosis, and edema associated with the affected arteries. These arterial lesions became evident in rats at and after the age of 24 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coronary arterial abnormalities in hyperlipidemic rats with renal failure. 802 73

Six boys and six girls aged under 3 years with asymptomatic hematuria and/or proteinuria were found and renal biopsies were performed from 1 month to 10 years after the discovery. Light microscopy uncovered 4 cases of focal segmental glomerulosclerosis (FSGS), 3 cases of diffuse mild mesangial proliferation, and 5 cases of minor glomerular abnormalities. Immunofluorescent studies did not show any significant depositions. Electron microscopy revealed diffuse thinning of the glomerular basement membrane (GBM) in 2 cases, and segmental thinning of the GBM in 8 cases, including 2 cases of FSGS found in the light microscopy. Four cases, including 2 cases of FSGS, had irregular thickening of the GBM and splitting of the lamina densa. Two cases of FSGS did not have GBM abnormalities. The significance of GBM abnormalities in children with asymptomatic hematuria and/or proteinuria under 3 years of age needs to further evaluated.
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PMID:[Asymptomatic hematuria and/or proteinuria in children under 3 years of age: clinicopathological evaluation]. 808 72

We performed a detailed clinical review and pathologic analysis of the kidney biopsies of 134 children with nephrotic syndrome or asymptomatic proteinuria. This analysis challenges some of our concepts about the classification of conditions associated with these disorders. The presence of focal segmental sclerotic lesions does not define a unique disorder in childhood. Some children with such lesions will have unaffected glomeruli that are ultrastructurally completely normal. These patients, predominately black adolescents, present either with nephrotic syndrome or asymptomatic proteinuria. We classify this disorder as primary focal segmental glomerulosclerosis (FSGS) and have never found it to recur after transplantation. Most other children with FSGS have 1 of 2 specific glomerulopathies. Those with minimal change have generalized fusion of podocyte foot processes. Those with mesangial proliferation have similar foot process changes combined with mesangial expansion and proliferation and, frequently, thinning of the lamina densa and tubuloreticular inclusions. The presence of segmental lesions in these glomerulopathies appears to be nothing more than a marker of severity. Children with these glomerulopathies are generally younger white children, virtually all of whom have nephrotic syndrome. These disorders have a strong propensity to recur after transplantation. The presence of mesangial labeling of IgM or C1q has no significance in any of these 3 disorders. The classification of disorders associated with nephrotic syndrome or asymptomatic proteinuria must concentrate less on the presence or absence of focal sclerosis and more on the histologic appearance of the rest of the glomeruli.
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PMID:The nonspecificity of focal segmental glomerulosclerosis. The defining characteristics of primary focal glomerulosclerosis, mesangial proliferation, and minimal change. 906 87

Thin glomerular basement membrane (GBM) nephropathy, also called familial benign hematuria, is characterized by chronic hematuria and uniform thinning of the lamina densa of the glomerular basement membrane. It generally holds an excellent renal prognosis. Alport syndrome in early stages can also show attenuation of the GBM; conversely, renal insufficiency has been reported in familial benign hematuria. To discern early Alport syndrome from thin GBM nephropathy, we carried out a prospective epidemiological study in which 19 normotensive and non-azotemic adult patients with chronic microscopic (18 of 19) and macroscopic (1 of 19) hematuria and biopsy-proven thin GBM nephropathy were followed for a median of 12 years (range 9 to 15 years). Renal biopsies of thin GBM patients at entry showed an increased incidence of focal global glomerulosclerosis when compared to disease controls as IgA nephropathy (P = 0.047) and normal renal tissue (P = 0.0075). All renal biopsies showed the presence of the Goodpasture antigen when tested immunohistochemically. Presence of Alport syndrome was excluded clinically as none of the patients had complaints of hearing loss or abnormalities by audiography and ophthalmology. At the end of follow-up, the incidence of hypertension in thin GBM nephropathy (35%) exceeded that of healthy clinical controls (P = 0.048), and one hypertensive patient developed mild renal failure. In the normotensive patients, the glomerular filtration rate at follow-up as measured by inulin clearance was reduced in three out of seven; these were over 50 years of age. Although no family members were known to have renal disease at inclusion, within four families six elderly first degree relatives had developed unexplained renal insufficiency at the end of follow-up. Thus, thin GBM nephropathy predisposes to premature glomerular obsolescence, leading in time to increased incidences of hypertension and late onset renal insufficiency.
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PMID:Thin GBM nephropathy: premature glomerular obsolescence is associated with hypertension and late onset renal failure. 915 Apr 78

It has been reported that circumferential mesangial interposition (CMI) is an important morphological feature suggesting the progression of glomerulosclerosis in glomerular disease. The relation between CMI and its associated lesions was investigated in various renal diseases by electron microscopy. In 276 patients, of whom the glomeruli were observed by electron microscopy, CMI was observed non-specifically in 48 patients with various glomerular diseases (IgA nephropathy, 11; non-IgA glomerulonephritis, 1; membranoproliferative glomerulonephritis, 8; membranous nephropathy, 5; lupus glomerulonephritis, 12; toxemia of pregnancy, 2; diabetic nephropathy, 7; mitomycin nephropathy, 1; and Seckel's dwarfism patients, 1). The glomeruli with CMI showed a marked increase in mesangial matrix, as well as various grades of mesangial cell proliferation. Mesangiolysis associated with subendothelial widening was observed in a lesion of CMI in most cases. This phenomenon appears to be an initial alteration that conducts proliferated cells to the peripheral portion of a capillary loop. Localized severe thinning of the glomerular basement membrane was frequently combined with CMI, particularly in IgA nephropathy patients. Endothelial cells were occasionally interposed into the widened subendothelial space. Subendothelial deposits were noticed in the CMI lesion, particularly in MPGN patients. In conclusion, in the process of glomerulosclerosis progression in various glomerular diseases, lytic and edematous changes initially occur in the mesangio-subendothelial system (mesangiolysis and subendothelial widening), then proliferating mesangial cells extend into the widened space (between GBM and endothelial cells), and reach the peripheral portion of a capillary loop.
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PMID:[An electron microscopic study of circumferential mesangial interposition in various renal diseases]. 965 10


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