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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renal allograft is host to a number of injuries and all its structural components are prone to damage. The glomeruli respond to these varied stimuli in many ways. The fibrinoid necrosis, thrombosis, and polymorphonuclear cell exudation that accompany hyperacute or accelerated rejection are well-recognized. The transplant may also be afflicted by forms of de novo or recurrent glomerulonephritis. Apart from these, there are other patterns of reaction. The mesangium is often the site of a rapidly reversible change; it expands readily. Arterial changes initiate ischemia and collapse of glomerular capillary spaces. Glomerulitis accompanies cases of acute rejection, but when seen as a predominant feature, usually antedates chronic rejection. Heavy proteinuria may be associated with profound alterations in the peripheral capillary basal lamina including irregular thickening, interposition of mesangial cell cytoplasm, and lamellation. Allografts with these glomerular changes eventually fail.
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PMID:Glomerular changes in renal allografts. 351 May 33

Renal involvement in legionnaires' disease is a well-known, yet incompletely understood, complication. Manifestations of renal involvement include proteinuria, hematuria, pyuria, cylindruria, and azotemia. Previous cases of legionnaires' disease with renal involvement have shown pathophysiologic changes consistent with acute tubulointerstitial nephritis or acute tubular necrosis. A toxic metabolite produced by Legionella pneumophila has been theorized to produce a vasoconstrictive effect on the renal microvasculature, leading to ischemia and renal dysfunction. The case reported here is unique in that the patient presented with interstitial nephritis in the absence of pulmonary signs or symptoms.
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PMID:Interstitial nephritis in a patient with Legionnaires' disease. 380 71

We assessed the effects of preservation on subsequent graft function by measuring and comparing creatinine and fractional protein clearances in 18 live-related (LR) and 38 cadaver-donor (CD) grafts, the latter selected on the basis of short warm ischemia times (less than 5 mins) and stable donor hemodynamic status prior to organ recovery. CD recipients with immediate graft function had lower initial creatinine clearances and greater fractional protein clearances than LR recipients. The role of preservation in producing greater fractional protein clearance was suggested by the observation of time-dependent increasing proteinuria during continuous hypothermic perfusion of four human CD kidneys and the significant correlation between the initial degree of proteinuria at onset of diuresis and the duration of cold preservation of those CD kidneys with immediate function. One-half of CD grafts, however, manifested acute renal failure (ARF) after implantation and in these grafts no correlation between cold preservation duration and fractional protein clearance at onset of diuresis was noted. Development of ARF in CD grafts was associated with still lower creatinine clearances, but higher fractional protein clearances during the first week of diuresis. These effects of preservation and those of preceding ARF on fractional protein clearances were no longer noted 2 wk after onset of diuresis in nonrejecting CD grafts. These observations suggest the presence of preservation-induced injury to grafts even when "immediate function" occurs.
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PMID:Some effects of preservation and acute renal failure on function and proteinuria of renal transplants. 633 80

The renal transplant vascularity of 72 patients was investigated by intravenous digital subtraction angiography (IV DSA). The procedure was combined with selective venous renin sampling of the transplant and native kidneys to identify the source of hypertension in these patients. Abnormalities were found on IV DSA examination in 26 patients, of whom 7 had graft artery stenosis, 7 had diffuse intrarenal narrowing, 9 had lower pole ischemia, and 3 had aneurysmal dilatation. The combined outpatient procedure was well tolerated by all patients with no complications nor incidence of proteinuria.
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PMID:Digital subtraction angiography in renal transplant recipients. 636 Mar 60

To determine whether preexistent glomerular injury and the nephrotic syndrome increase renal susceptibility to ischemic renal injury, normal rats and rats with either experimental minimal-change disease (Adriamycin nephropathy) (AN) or membranous nephropathy (passive Heymann nephritis) (PHN) underwent renal functional and histologic studies under either basal conditions or 18 h after bilateral renal artery occlusion (over 30 min). Prior to renal ischemia AN and PHN rats had minimally depressed glomerular filtration rate (GFR), normal (AN) or increased (PHN) renal blood flow (RBF), heavy proteinuria, hypoalbuminemia, decreased urine sodium excretion, extensive glomerular foot process fusion, and intratubular hyalin cast formation. Losses of GFR in response to ischemia were comparable among the three groups of rats (controls, 0.29; AN, 0.28; PHN, 0.25 ml X min-1 X 100 g body wt-1) despite prevailing differences in postischemic hemodynamics. Neither light nor transmission electron microscopy showed any differences in the degree of ischemic renal injury. These results suggest that 1) glomerulopathy and the nephrotic syndrome do not significantly increase renal susceptibility to ischemic renal injury; 2) the syndrome of acute renal failure that occurs in patients with minimal-change glomerulopathy is not due to a marked susceptibility of these kidneys to clinically occult ischemic events; and 3) foot process fusion is probably not a pathophysiologically significant lesion in ischemic acute renal failure, as previously suggested.
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PMID:Glomerulopathy does not increase renal susceptibility to acute ischemic injury. 670 61

For the calculation of the donor influence on the results of renal grafting, all non-renal causes of transplant failure must be excluded. The following criteria for the selection of a suitable kidney donor were found: the urine production of the donor in the last hour before nephrectomy should amount to at least 200 ml and the age difference between donor and recipient should be not more than 20 years. Proteinuria, a high serum creatinine level, vascular anomalies and a long operation time for vascular anastomosis were unfavourable. The preservation time, the warm ischemia time and the sex of the donor have little effect. If no rejection crises occurred within the first 3 weeks after transplantation, the transplant survival rate increased from 45% to 71%.
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PMID:[Choice of donor and the results of renal grafting (author's transl)]. 679 34

The protective effect of Collins or Sacks solutions was reduced after warm ischemia in preserved and reperfused dog kidneys. The degree of the developed pathologic alterations was connected with the length of the warm ischemic period. Functional changes as decrease of microcirculation and proteinuria and structural sequences as edema and diverse disintegration in glomeruli and tubuli were produced.
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PMID:[Value of organ preservation with Collins-3 and Sacks II solutions of warm ischemic and re-perfused kidneys]. 700 37

In two groups of nonpregnant guinea pigs, uterine ischemia was produced by banding the uterine arteries and transecting the ovarian arteries. Since this procedure prevented the increase of uterine blood supply that normally occurs during pregnancy, uteroplacental ischemia resulted when the animals became pregnant. Intraarterial blood pressures were recorded immediately after surgery and again near term. Hypertension, proteinuria and elevated creatinine levels (changes similar to those of human preeclampsia) were consistently found near term in all of the banded animals that became pregnant. These findings support the view that it is possible to develop a toxemia model in the guinea pig.
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PMID:Experimental toxemia in the pregnant guinea pig (Cavia porcellus). 705 72

In this analysis of 43 patients with IgA nephropathy, renal morphology was correlated with clinical data. Gross hematuria and mild proteinuria were typical among younger patients. Among older individuals the clinical spectrum was wider. A comparison with data previously obtained from the normal population indicated that disease-related glomerular sclerosis was present in 1/3 of initial biopsy specimens. The prevalent pattern of glomerular sclerosis was that of global tuft collapse, the type of sclerosis known to result from ischemia. Intrarenal vascular sclerosis was present in 1/3 of initial biopsies. Follow-up specimens from 6 patients showed progression of glomerular sclerosis, vascular sclerosis or both. Hypertension occurred in over 1/4 of patients. It is proposed that progressive renal damage in IgA nephropathy may not be solely immunologically mediated. Glomerular sclerosis may also be mediated by vascular sclerosis, or alterations in intrarenal hemodynamics in glomerulonephritis may have a direct damaging effect on both the glomerulus and the intrarenal vasculature.
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PMID:Intrarenal vascular sclerosis in IgA nephropathy. 714 32

Rat kidneys were perfused with anti-intercellular adhesion molecule-1 (anti-ICAM-1) monoclonal antibody prior to allotransplantation. In the two strain combinations examined, LEF-to-WKAH transplants resulted in accelerated graft loss, and no prolongation of graft survival. The accelerated graft loss was the result of frequent occurrence of necrotizing arteritis within the grafts. In contrast, TO-to-WKAH transplants resulted in no change in graft survival and no arteritis. Necrotizing vasculitis in the LEJ-to-WKAH grafts was characterized by fibrinoid necrosis, collection of cellular infiltrates and serum macromolecular protein entrapment. The F(ab1)2 form of anti-ICAM-1 antibody partially preserved the antibody's capacity to accelerate graft loss. Therefore, although endothelial injury by Fc-mediated cytotoxicity may be involved in vascular damage, other mechanisms also come into play. The amount and distribution pattern of ICAM-1 antigen were identical in both TO and LEJ strains. Intravenous anti-ICAM-1 antibody administration combined with lipopolysaccharide, Poly(I)-Poly(C), warm ischemia to the kidney, or subcutaneous immunization with allogeneic spleen cells, but without renal transplantation, did not generate necrotizing vasculitis or proteinuria. These observations plus our previous data on the rat liver transplantation model clearly show that graft perfusion with anti-ICAM-1 monoclonal antibody invokes extensive vascular damage within allografts by Fc-mediated and Fc-independent mechanisms, depending on the donor-to-host combination.
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PMID:Strain combination-dependent genesis of necrotizing arteritis in anti-ICAM-1 antibody-perfused renal allografts in the rat. 778 89


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