Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is considerable circumstantial evidence relating neoplasia to glomerular injury. Recently, more convincing evidence has been derived from the demonstration of tumor-associated antigen or antibody to such antigen, in relation to glomerular basement membranes in four patients with glomerular injury and cancer. The most common form of glomerulopathy reported in patients with carcinoma has been membranous glomerulonephritis. However, increased mesangial cells and matrix have also been found in some patients with hematuria and progressive renal failure. In contrast, most patients with Hodgkin's disease and glomerulopathy have had the minimal lesion-type nephrotic syndrome, which has usually responded to successful treatment of the Hodgkin's disease. Glomerular abnormalities have also been reported with chronic lymphocytic leukemia, lymphosarcoma, Waldenstrom's macroglobulinemia, and benign tumors. When there is no apparent cause, proteinuria with or without hematuria or impaired renal function should suggest the possibility of associated neoplasia, particularly in elderly patients.
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PMID:Glomerular injury in patients with neoplasia. 18 Aug 69

A series of 29 cases of amyloidosis of the alimentary tract is reported. Five cases (17%) were primary amyloidosis; 14 cases (48%) were amyloidosis secondary to other diseases (such as chronic inflammatory and neoplastic diseases); 10 cases (35%) were amyloidosis of the heredo-familial type connected with Familial Mediterranean Fever. In 23 patients (79%) the diagnosis was established by biopsies, and in 6 more cases on autopsy. Gastrointestinal involvement was found in all age groups. Gastro-enterologic complications observed in the present series include: diarrhea, malabsorption, ileus and gastrointestinal bleeding. In addition other conditions such as jaundice (3 cases), esophagitis and acute hemorrhagic pancreatitis were observed. In 22 patients proteinuria was observed and in 13 patients the nephrotic syndrome. Among 17 patients, in 11 the clinical picture before death was that of terminal renal failure. The survival after diagnosis among 14 patients reached 4 years in 9 cases, and 19 years in one case. The diagnostic value of the rectal biopsy is emphasized.
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PMID:[Gastrointestinal amyloidosis]. 18 89

The examples of tubular proteinuria, postobstructive diuresis, tubular function in terminal renal failure and the hereditary defects of tubular transport mechanisms are used to demonstrate the difficulty in elucidating defects of renal membrane transports in man. She is caused by the impossibility of applying the appropriate techniques to evaluate membrane functions in man and by the complexity of human disease. The rapidly growing knowledge of physiologic membrane functions in the kidney should however enable some progress in the field of human pathophysiology in a not too remote future.
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PMID:[Pathophysiology of the membrane function in the kidney]. 18 5

In 26 cases of myelofibrosis, the authors investigated for possible renal impairment that can be appraised from the usual clinical, laboratory, and roentgenographic signs. No anomalies were demonstrated in 12 of these cases. In 14 (or 53%) of the patients, some anomaly was discovered : essentially proteinuria with minor alteration of renal function, but also, two cases of poorly functioning left kidney evidenced on intravenous urograms, one case of acute anuric renal failure connected with hyperuricemia, one case of hypokalemic tubulo-interstitial nephritis, and one case of glomerulonephritis with, nephrotic syndrome. This study, when compared to the literature, indicates that besides nephropathy specific to myelofibrosis and attributed to myeloid metaplasia in the kidney, serious consideration must be given to lesions due to (1) compression of the left kidney by the enlarged spleen, (2) urate precipitation in the urinary passages, and (3) a possible glomerular disorder whose mechanism remains undefined.
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PMID:[Renal lesions in myelofibrosis (author's transl)]. 22 98

Metabolic balance studies were carried out in 17 unselected patients with acute myeloid leukaemia. Widespread metabolic disturbances were observed. Serum Na fell below 135 mmol/1 in 14 patients (82%) and 11 patients (64%) developed hypokalaemia. An increased osmolal clearance caused by a release of electrolyte and blast cell waste (i.e. urea, urate, etc.) during chemotherapy appeared to be the principle cause of natriuresis and hyperkaluria. Seven patients had proteinuria before and eight others developed it during antileukemic therapy. Nine patients (53%) developed proximal renal tubular dysfunction with aminoaciduria, hyperphosphaturia and incomplete reabsorption of urate. No significant relation was found between this widespread glomerulo-tubular dysfunction and lysozymuria. We suggest that antileukaemic drugs release unidentified substances from blast cells which are toxic to the kidney. Metabolic alkalosis in six patients (35%) was probably related to volume depletion and hypokalaemia, while two patients developed acidaemia with the onset of renal failure. Hypocalcemia in seven patients (41%) had a multifactorial basis: hyperphosphaturia, septicaemia, malnutrition and cytotoxic drugs were among the probable causes.
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PMID:Metabolic disorders in acute myeloid leukaemia. 28 Mar 62

The risk to the transplanted kidney of vesicoureteric reflux was evaluated in 150 consecutive first cadaveric renal allografts surviving for over three months. Of the 119 (79 per cent) allografts studied by micturating cystography 29 (24 per cent) were shown to reflux. The presence of reflux was associated with urine leakage and reoperation, and with ureteric insertion involving a short intramural tunnel. Graft failure (graft nephrectomy or death from renal failure) occurred in 14 of 29 refluxing grafts as compared to 14 failures in 90 nonrefluxing grafts (P less than 0.01). Graft failure in the refluxing group was typically slow, and commonly associated with proteinuria, microscopic hematuria, hypertension and a biopsy appearance of mesangiocapillary glomerular change. Urinary infection, though frequent (69 per cent), was not more common in the group with than in that without reflux. Vesicoureteric reflux is an important cause of late renal-graft failure.
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PMID:Risks of vesicoureteric reflux in the transplanted kidney. 32 32

Acute pulmonary silicoproteinosis, massive proteinuria and fatal renal failure developed in a 23 year old male sandblaster. Examination of the kidney by immunofluorescence revealed granular deposits of immunoglobulin M (IgM) and the third component of complement (C3) along the glomerular basement membrane. Light microscopy disclosed mild proliferative glomerulonephritis with loss of colloidal iron staining for sialoprotein, and electron microscopy disclosed an increased density of epithelial cytoplasm, altered lysosomes and endothelial cell microtubular structures. The silicon content of the kidney was 264 parts per million (ppm), but particles of silicon were not demonstrated by electron microscopy. No primary or systemic causes of renal diseases were elucidated. The renal dysfunction apparently resulted from acute renal silicon toxicity, a new complication of acute pulmonary silicoproteinosis.
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PMID:Massive proteinuria and acute renal failure in a patient with acute silicoproteinosis. 34 91

Analgesic abuse is a major public health hazard in Australia, and analgesic nephropathy with consequent terminal renal failure is the underlying cause in 20% of the patients requiring dialysis and transplantation. Analgesics are invariably taken in the form of compounds and mixtures. In the aspirin-phenacetin-caffeine (APC) mixture, aspirin appears to be the major nephrotoxic agent and phenacetin appears to play a secondary and synergistic role. The renal disease associated with abuse of analgesics is characteristic and is part of a much wider clinical syndrome, the analgesic syndrome, which includes peptic ulcer disease (35%), anemia (60 to 90%), hypertension (15 to 70%), ischemic heart disease (35%), psychological and psychiatric manifestations, pigmentation, and possible gonadal- and pregnancy-related effects. The primary lesion in analgesic nephropathy is renal papillary necrosis (RPN), and this is a nephrotoxic effect common to all nonsteroid antiinflammatory agents. The most important factor in the management of patients with analgesic nephropathy is the cessation of analgesic abuse, and this leads to improvement and stabilization of renal function. A small proportion of patients will, however, deteriorate in relation to accelerated hypertension, persistent proteinuria, ischemic heart disease, and complications leading to nephrectomy. Patients with analgesic nephropathy are poor risk patients and have a poor prognosis, even after dialysis and transplantation.
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PMID:Analgesic nephropathy: etiology, clinical syndrome, and clinicopathologic correlations in Australia. 36 34

Forty consecutive patients whose biopsies showed focal and segmental sclerosis were studied for 6 to 16 years to establish the long-term prognosis of this group of patients. By the end of a decade 21 were dead, on regular dialysis or transplanted; only one death was unrelated to renal failure. A further 8 patients had a GFR of less than 60 ml/min/1.73 m2. Only 11 patients had normal renal function, and of these eleven only four had no urinary abnormality. Actuarially calculated survival was 75% at 5 years, 50% at 10 years, and 38% at 15 years. There was no difference between the 28 adults and the 12 children in terms of evolution. Patients with a nephrotic syndrome at presentation had a poorer prognosis than those never nephrotic. Twenty nephrotic patients were treated with prednisone, and 14 of these with cyclophosphamide in addition. One patient responded with loss of proteinuria within two months to both drugs, and another lost proteinuria when treated with cyclophosphamide. Thirteen patients received allografted kidneys; a nephrotic syndrome recurred in three patients, with histological evidence of recurrent disease in two.
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PMID:The long-term prognosis of patients with focal segmental glomerulosclerosis. 36 7

The role played by the macrophage in the development of injury in rabbit nephrotoxic nephritis (NTN) has been assessed by electron microscopy and glomerular culture of renal tissue obtained by several biopsies during the course of the disease. These observations have been correlated with the other immune, cellular, and biochemical events occurring in the glomerulus, ie, deposition of immunoglobulin and complement, proteinuria, polymorphonuclear leukocyte (PMN) exudation, fibrin deposition, crescent formation, and renal failure. A biphasic macrophage accumulation was detected, corresponding to the heterologous and autologous phases of the disease. In the autologous or crescentic phase, macrophages accumulated within the glomerular tuft from Day 5; their appearance coincided with the accumulation of PMN and development of proteinuria. Fibrin deposition in Bowman's space, which commenced on Days 6 and 7, was rapidly followed by the migration of macrophages from the glomeruli into Bowman's space. Within Bowman's space, macrophages were observed to phagocytose fibrin, transform into epithelioid and giant cells, and accumulate to form a substantial proportion of the cells forming the crescent. The inflammatory process of PMN exudation, macrophage accumulation, fibrin deposition, and crescent formation and the degree of renal failure reached a maximum by Days 12 to 14. Thereafter, resolution of the inflammatory process occurred so that by Day 40 macrophages had disappeared from the glomeruli. However, varying degrees of glomerular damage and renal failure persisted, occurring largely as a result of glomerulosclerosis and sclerosis of crescents. The tissue culture studies also demonstrated mesangial cell proliferation during the inflammatory process but did not show any abnormality of epithelial cell activity. This study demonstrates that the macrophages participate in NTN by accumulating in damaged glomeruli then migrating into Bowman's space (probably in response to fibrin deposition) where they undergo granulomatous transformation and accumulate, contributing to crescent formation.
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PMID:The macrophage in the development of experimental crescentic glomerulonephritis. Studies using tissue culture and electron microscopy. 37 9


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