Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal failure due to combined acute interstitial nephritis and minimal-change glomerulopathy is reported in two patients after fenoprofen therapy. In the interstitial infiltrates, T lymphocytes predominated over B lymphocytes in a ratio of four to one. The majority of B lymphocytes present were IgE-bearing cells. Among the T cells, the ratio of cytotoxic/suppressor cells to helper-inducer cells was three to one. Repeated renal biopsy in one patient after steroid-induced clinical remission demonstrated resolution of the inflammatory infiltrate and restoration of normal glomerular foot processes. The theoretic and practical implications of these findings are discussed.
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PMID:T and B lymphocyte subsets in fenoprofen nephropathy. 660 49

Vesicoureteral reflux is an anatomic abnormality, mostly affecting a pediatric population, which may be the second leading cause of end-stage renal failure. Most cases of reflux are due to abnormalities in the insertion of the ureters into the bladder, either congenital or acquired. Most commonly, VUR is discovered during routine evaluation of urinary tract infections, but may also be present in patients with severe hypertension or chronic renal failure. The diagnosis is confirmed radiologically, utilizing either voiding cinecystography or radioisotopic methods. VUR can result in renal failure through scarring secondary to 'chronic pyelonephritis' or through a glomerulopathy, possibly immune in origin. In most series, the glomerulopathy is felt to be the cause of the end-stage renal failure. Treatment of VUR includes conservative (medical) management with the hope that maturation of the ureterovesical junction will cure reflux. Surgical therapy is reserved for those patients in whom this maturation is not expected to occur or in those whose urinary infections cannot be controlled. In those patients who have developed the glomerulopathy secondary to VUR, surgery may not halt the progression of the renal disease. VUR in a transplanted kidney may result in a higher risk of loss of the graft due to glomerulopathy or chronic rejection.
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PMID:Vesicoureteral reflux and reflux nephropathy. 676 61

The relations among renal function, proteinuria, and glomerular lesions were studied in 54 patients with reflux nephropathy. The clinical course to end-stage renal disease was not appreciably altered by late surgical correction of the reflux, occurrence of urinary tract infection, or hypertension. All patients with progressive renal disease had significant proteinuria. Mesangial glomerular lesions can occur in the absence of proteinuria detectable by routine analysis, whereas lesions similar to those seen in idiopathic focal sclerosing glomerulopathy were present in the renal biopsies from proteinuric patients. Deposition of immunoproteins was limited to glomeruli undergoing sclerosis. Similarly, electron-dense deposits were confined to areas of mesangial alterations. Our results suggest that mesangial alterations occur early in the course of reflux nephropathy and may lead to the development of focal sclerosis. At later stages, counterproductive mechanisms of adaptation to the loss of viable nephrons might result in an acceleration of the clinical course to renal failure.
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PMID:The progression of vesicoureteral reflux nephropathy. 699 78

We analyzed clinical and pathologic data from 36 recipients of 38 renal allografts who developed nephrotic syndrome following transplantation. Three groups were identified on the basis of histologic changes in the graft, and each group had a distinct clinical course. Nine grafts (23.7%) had recurrent glomerulonephritis (GN) (5 membrano-proliferative, 4 focal glomerulosclerosis) and developed nephrotic syndrome at 5.1 months (mean) posttransplant. Renal function deteriorated rapidly, with a 2-year graft survival of 29.7%. Four grafts (10.5%) with de novo GN (3 epimembranous, 1 minimal change) developed nephrotic syndrome at 32 months posttransplant, and all functioned for more than 3 years. Twenty-five grafts (65.8%) had allograft glomerulopathy with the onset of nephrotic syndrome at 9.1 months posttransplant and a 2-year graft survival of 66.6%. The differences in duratin of graft function between grafts with allograft glomerulopathy and recurrent GN (P < 0.01) and in graft survival rates at 2 years among the three groups (P < 0.05) are statistically significant. This analysis indicates that allograft glomerulopathy is the most common cause of kidney transplant nephrotic syndrome. Membranoproliferative GN and focal glomerulosclerosis may recur soon after transplantation and rapidly progress to renal failure in marked contrast to grafts with either de novo epimembranous nephropathy or minimal glomerular change, lesions that are compatible with prolonged graft function.
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PMID:Kidney transplant nephrotic syndrome: relationship between allograft histopathology and natural course. 700 10

The 1,205 renal biopsies performed at The Hospital for Sick Children, Toronto, were reviewed to identify membranous glomerulopathy. Fourteen patients had a clinicopathologic diagnosis of idiopathic membranous glomerulopathy. Typical thickening of glomerular capillary basement membranes, a spike-and-dome pattern, and subepithelial electron-dense deposits were noted. Strong deposits of IgG and weaker deposits of C3, IgM, and IgA were present in glomeruli. Stages of membranous glomerulopathy on electron microscopy were I in one biopsy, II in nine biopsies, and III in four biopsies. Two additional biopsies from one child initially showed minimal lesion-type disease; later, a third showed membranous glomerulopathy. At presentation 11 patients had nephrotic syndrome, seven had hypertension, and eight had hematuria. Now four are in remission, seven have active disease with normal renal function, and three have renal failure. Patients with hypertension tended to do worse than those without. Age at onset, presence of nephrotic syndrome or hematuria, and administration of steroids or immunosuppressive drugs did not adversely affect outcome. Furthermore, clinical outcome did not correlate with stage of disease. Hence pathologic and most clinical features do not predict long-term prognosis in children with membranous glomerulopathy.
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PMID:Idiopathic membranous glomerulopathy in Canadian children: a clinicopathologic study. 713 Nov 40

A patient with chronic Gaucher's disease is described who developed glomerulopathy 24 years after splenectomy terminating in renal failure. The pathological changes of this very rare complication of Gaucher's disease are described. The few similar cases reported in the literature are reviewed and the possible pathogenetic pathways discussed.
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PMID:Renal involvement in Gaucher's disease. 730 91

Structural alterations in the kidneys of 40 patients deceased from carbon tetrachloride (CCl4) poisoning were examined. All the patients had died with severe acute hepatic and renal failure. The authors found that it was consecutively developing hydropic and protein dystrophy of both proximal and distal tubules which accounted for acute renal failure. Changes in the glomeruli of the type of membranous glomerulopathy were also found. In the authors' opinion, the main cause of these alterations of the kidneys was presumably severe hepatic insufficiency with metabolic and immune disturbances.
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PMID:[Morphological changes in the kidneys after carbon tetrachloride poisoning]. 737 96

It has recently been suggested that immunotactoid glomerulopathy be separated from much more common fibrillary glomerulonephritis by ultrastructural features of highly organized immune deposits containing tubules of more than 30 nm in diameter. We report and discuss the results of a light, immunofluorescence and electron microscopic study of a needle renal biopsy from a 75-year-old, non-insulin dependant diabetic female presented with nephrotic syndrome, hypertension and a progressive renal failure. A unique coexistence of nodular glomerulosclerosis, as traditionally ascribed to diabetes with a peculiar type of immunotactoid glomerulopathy was confirmed by the exclusion of amyloidosis, monoclonal gammopathies, systemic autoimmune diseases and cryoglobulinemia. Mesangial, scattered subepithelial and segmentally prominent subendothelial immune deposits were found highly organized in mostly parallel arrays of 40 to 91 nm thick tubules. The average thickness of 67 nm exceeds the average diameter of tubules in all other 11 published cases of immunotactoid glomerulopathy to date. By immunofluorescence, predominantly capillary wall, thick, ribbon-like glomerular deposits contained IgG, IgM, kappa and lambda light chains of equal intensity, C3, C4 and fibrin related antigens. Mild to moderate glomerular cell proliferation associated with nodular sclerosis has been assumed to be causally related to immunotactoid deposits.
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PMID:Immunotactoid glomerulopathy with unusually thick extracellular microtubules and nodular glomerulosclerosis in a diabetic patient. 747 81

Studies and textbooks from the 1970s and early 1980s list focal-segmental glomerulosclerosis (FSGS) as accounting for 10% to 15% of cases of idiopathic nephrotic syndrome in adults, although a recent review by D'Agati (Kidney Int 46:1223-1241, 1994) reported an approximately sevenfold increase in the incidence of FSGS from 1974 to 1993 in an active renal biopsy practice. To investigate possible changes in the incidence of FSGS in our renal biopsy practice, we reviewed reports from all nontransplant, adult (> or = 18 years) renal biopsies received in our laboratory from 1974 to 1993, which comprised 7,420 cases. All diagnoses of membranous nephropathy (MN), minimal change nephropathy (MCN), and FSGS made in each year were compiled; cases clearly or suspicious of being secondary to an underlying systemic disease, glomerulonephritis, or drug reaction were excluded. Relative frequencies of MN, MCN, and FSGS among these three diseases and among all biopsies were calculated for each year of the study. Regression analysis showed a significant (P < 0.001) increase in the odds of a diagnosis of FSGS over the study period: 7.6% per year among all biopsies and 6.8% per year among cases of MN, MCN, and FSGS only. Among all biopsies, the yearly incidence of FSGS increased from 4.0% +/- 0.6% (mean +/- SD) during the period between 1974 and 1979 to 12.2% +/- 2.0% during the period from 1987 to 1993. The odds of a diagnosis of MN (mean yearly incidence, 9.5% +/- 1.9%) did not vary significantly over the study period while the odds of a diagnosis of MCN (mean yearly incidence, 4.0% +/- 1.2%) declined at a rate of 2.2% per year (P < 0.03). Frequencies of diagnosis of MN, MCN, and FSGS by two pathologists were almost identical. Review of available slides from cases of FSGS revealed 21 (none before 1980) with characteristic histologic features of the collapsing glomerulopathy (CG) variant of FSGS. No more than four cases of CG were observed in any year of the study, and CG accounted for 4.7% of total FSGS cases for which diagnostic slides were available. Compared with 42 patients with non-CG FSGS, the CG cohort showed a greater percentage of black patients (86% v 38%), significantly higher mean levels of serum creatinine (3.8 +/- 2.7 mg/dL v 1.9 +/- 1.5 mg/dL) and urinary protein (14.3 +/- 9.6 g/24 hr v 7.7 +/- 5.8 g/24 hr) at the time of renal biopsy, and a greater likelihood of and more rapid progression to end-stage renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Increasing incidence of focal-segmental glomerulosclerosis among adult nephropathies: a 20-year renal biopsy study. 748 26

The magnitude of type II diabetic nephropathy dilemma is observable in the growing number of diabetic patients with end-stage renal lesion receiving various modalities of treatment. Progressive glomerulopathy associated with proteinuria and hypertension is strongly causative of renal failure and mortality in diabetic patients. Besides hypertension, diabetes exceeds all other glomerulopathies in causing end-stage renal failure. Alterations in glomerular structure and function observed in diabetic patients are implicated in the development and progression of renal derangement. Diabetic glomerulosclerosis, an aggregate of structural and functional perturbations of the kidney, is indicated by alterations in the accumulation of extracellular matrix components, The pathology, epidemiology, risk factors, and other dependent variables may throw some light in the pathogenetic mechanisms and the prevention, treatment, and management modalities of type II diabetic nephropathy.
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PMID:Type II diabetic nephropathy in perspective. 773 45


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