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PubMed2006

Cholesterol crystal embolism: diagnosis and treatment.

Cholesterol crystal embolization (CCE) is a dreaded complication of radiology, vascular surgery, and/or anticoagulation in patients with atherosclerosis and ulcerated aortic plaques. It also represents a cause of early graft failure and of poor results of renal artery surgery. Crystals lodge in small caliber renal arteries, where they induce early, transitory thrombosis followed by delayed, definitive obstruction by endarteritis, accompanied by evidence of inflammation and eosinophilia. Massive CCE leads to early oligoanuria. In subacute forms, renal insufficiency is often delayed by weeks or months following the triggering event. A third, chronic subset of CCE is easily mistaken for atherosclerotic renal ischemia and/or nephrosclerosis. The kidney is rarely the sole organ involved in acute/subacute forms, in which the central nervous system, the coronary arteries, the spinal cord, and the mesenteric and pancreatic blood supply compromise represent the main causes of death. Cutaneous, retinal, and muscle involvement allow diagnosis by inspection or scarcely invasive biopsies in about 80% of cases, whereas renal biopsy as the only diagnostic procedure is required in 20% of cases. Prevention is based on avoidance of endovascular radiology maneuvers, vascular surgery, and excess anticoagulation in atherosclerotic patients. Treatment of acute/subacute forms of renal insufficiency consisting of stopping anticoagulation and forbidding any new radiologic and/or vascular surgery procedure; treating hypertension with angiotensin 2 antagonists and vasodilators, strict volemic control by loop diuretics and ultrafiltration, along with parenteral nutrition and prednisone, has been credited with improved outcome. Iloprost may obtain favorable results. Statins definitely ameliorate the renal and patient's prognosis.

Diagnosis, Differential↗

PubMed2000

Expression of decorin, biglycan, and collagen type I in human renal fibrosing disease.

BACKGROUND: The extracellular matrix proteoglycans decorin and biglycan may have a pathogenic role in renal fibrosing disease via regulation of the activity of growth factors, such as transforming growth factor-beta, and effects on collagen type I fibrillogenesis. The expression of decorin and biglycan in human glomerular diseases characterized by mesangial sclerosis is unknown. METHODS: Decorin, biglycan, and collagen type I were localized immunohistochemically in human renal biopsy cases of amyloidosis (N = 18), diabetic nephropathy (N = 11), fibrillary glomerulonephritis (N = 5), immunotactoid glomerulopathy (N = 5), light-chain deposition disease (N = 4), idiopathic mesangial sclerosis (N = 4), and nephrosclerosis (N = 6), and in morphologically normal tissues obtained from tumor nephrectomies (N = 8). Decorin and biglycan mRNA synthesis was evaluated by in situ hybridization. RESULTS: Decorin and biglycan protein were not identified in normal glomeruli. Decorin accumulated in amyloid deposits, but not in deposits of fibrillary glomerulonephritis or immunotactoid glomerulopathy. Biglycan weakly accumulated in amyloid deposits, and both decorin and biglycan weakly stained mesangial nodules in cases of morphologically advanced light-chain deposition disease and diabetic nephropathy. In all analyzed cases, irrespective of the underlying disease, decorin and biglycan accumulated in glomeruli in areas of fibrous organization of the urinary space and in areas of tubulointerstitial fibrosis. Biglycan, but not decorin, accumulated in the neointima of arteriosclerotic blood vessels. Decorin and biglycan mRNA synthesis was detected at sites of proteoglycan accumulation in glomeruli, interstitium, and neointima. Collagen type I colocalized with decorin and biglycan deposits. CONCLUSIONS: Differences in extracellular matrix proteoglycan composition may be diagnostically useful in distinguishing morphologically similar diseases. Distinct patterns of proteoglycan expression may be related to modulation of specific growth factor activity in different glomerular diseases.

Amyloidosis↗

PubMed1998

Hemodialysis vascular access: variable thrombus-free survival in three subpopulations of black patients.

Hemodialysis vascular access-related problems account for most hospitalizations in chronic hemodialysis patients. Although some co-morbid risk factors for early fistula failures have been described, a great deal of unknown exists as to why access survival is favorable in some patients. In this longitudinal study, fistulae patency and thrombosis episodes were monitored from placement date in three groups of end-stage renal disease (ESRD) patients who have been on dialysis for > or =90 days. Thirty-six patients (29 male; 80%) with a mean age of 42+/-2 years were monitored. The groups consisted of eight patients with biopsy-confirmed focal segmental glomeruloscierosis (FSGS), 13 with acquired immunodeficiency syndrome-related nephropathy (human immunodeficiency virus [HIV]), and 15 with hypertensive ESRD (hypertensive nephrosclerosis [HTN]) who served as controls. Diabetics and patients aged > or =64 years were excluded. Twenty-five of 36 (69%) fistulae were prosthetic (AVG), while 11 (31%) were native (AVF). The FSGS group was more likely to have an AVG (87.5%), while 54% of the HIV group had an AVG. The thrombosis event rate was significantly greater among the FSGS patients (3/patient-year) than the HIV (0.15/patient-year) and HTN (0.5/patient-year) patients (P < 0.0001 and P < 0.002, respectively). The mean thrombosis-free duration for both AVG and AVF among the HIV and HTN groups were 318.5+/-17 days and 311.7+/-22.5 days, respectively. These were significantly greater than in the FSGS group (26.5+/-7 days; P < 0.0001). The cumulative 1-year patency rate for AVG among the HIV and HTN groups was 85% and 65%, respectively, while that of the FSGS group was 0%. Kaplan-Meier hazard analysis showed that all groups were at risk of access thrombosis as time progressed, but the FSGS group had the highest risk of access thrombosis, which began from the date of placement and increased exponentially with time. The increased thrombosis rate among the patients in the FSGS group correlated with their weight (R = 0.8, P = 0.003) and pre-ESRD 24-hour urinary protein excretion (R = 0.9, P = 0.001). The HIV status appeared to confer enhanced hemodialysis access survival. This may be related to the high rate of native fistulae placement and favorable vascular reactivity to shear stress. Accelerated atherosclerosis and small caliber vessels may be responsible for the poor fistulae outcome among the FSGS group. More studies will be necessary to further explore these findings.

AIDS-Associated Nephropathy↗

PubMed2001

Iron deposition in renal biopsy specimens from patients with kidney diseases.

This study was performed to investigate the correlation between clinical parameters and grading of iron deposition in renal biopsy specimens from 102 patients with various kidney diseases. Iron deposition in renal tissues was detected by Berlin blue staining. The extent of iron staining was semiquantitatively graded as negative (Fe(-)), grade 0, or positive (Fe(+)), including faint, grade 1; moderate, grade 2; or severe, grade 3, by light microscopy. Thirty-four of 102 patients (33%) showed positive iron staining. Fe(+) patients had various renal diseases, mainly consisting of 12 patients with immunoglobulin A nephropathy and 5 patients with benign nephrosclerosis. Mean arterial pressure (MAP), serum creatinine (sCr) levels, incidence of hematuria, and urinary N-acetylbeta-D-glucosaminidase (u-NAG) levels in Fe(+) patients were significantly greater than those in Fe(-) patients, and u-NAG levels correlated positively with the extent of iron deposition. Study patients were tentatively divided into two groups according to the extent of iron deposition: group A, patients with grades 2 and 3 staining, and group B, patients with grades 0 and 1 staining. In group A, MAP, sCr level, urinary protein excretion, and the incidence of hematuria were significantly greater than in group B. Our results suggest that the amount of iron deposition in renal tissue may contribute to the progression of chronic renal disease and may be an early and sensitive indicator of renal damage in certain renal diseases.

Acetylglucosaminidase↗

PubMed2002

A patient with apolipoprotein E2 variant (Q187E) without lipoprotein glomerulopathy.

Four apolipoprotein (apo) E variants have been reported to be associated with lipoprotein glomerulopathy (LPG), which is characterized by type III hyperlipoproteinemia (type III HLP) and proteinuria and frequently leads to nephrotic syndrome. We report the histologic findings in the kidneys of a type III HLP patient with an apo E variant, apo E Toranomon, in which the glutamine at residue 187 in apo E is substituted by glutamic acid (Q187E). The patient also had type 2 diabetes mellitus. No evidence of lipoprotein thrombi suggestive of LPG was detected, however, and the histologic diagnosis was diabetic nephrosclerosis. This unique case illustrates that not all apo E variants result in LPG, and the location of mutations in the apo E protein is one of the important determinants for the development of LPG.

Apolipoproteins E↗

PubMed2004

Possible mechanism for medial smooth muscle cell injury in diabetic nephropathy: glycoxidation-mediated local complement activation.

BACKGROUND: Although recent studies have emphasized the pathogenic role of intrarenal muscular arteries in patients with diabetic nephropathy, notice has not been taken of their pathological characteristics. We focused on medial smooth muscle cell (SMC) injury and the involvement of glycoxidation and complement activation. METHODS: Renal samples were obtained at autopsy from patients with diabetes mellitus (DM), patients with hypertension without renal involvement (n = 9), patients with benign nephrosclerosis (n = 7), and age-matched control subjects (n = 12). Patients with DM had glomerulosclerosis classified as severe (n = 9; DM-sev), moderate (n = 11; DM-mod), and minimal (n = 7). Renal samples were immunohistochemically determined. Activation of plasma complement from healthy subjects using advanced glycation end products (AGEs) also was performed. RESULTS: A marked SMC loss was noted in the media of patients with DM-sev and DM-mod. A membrane attack complex (MAC) observed in the area with SMC loss correlated well with the loss. Considerable carboxymethyllysine (CML), an oxidatively modified AGE, was deposited in the area with SMC loss in patients with DM-mod and DM-sev. Degrees of MAC deposition, SMC loss, and CML deposition were greater in the DM-sev group than the non-DM groups. Another oxidative product, acrolein, colocalized with CML. Plasma complements were not activated by AGE-modified bovine serum albumin in our in vitro assays, which included a complement hemolytic activity assay and determination of complement fragments, including C4d, C3bB, iC3b, and MAC. CONCLUSION: It is strongly suggested that medial SMC injury in intrarenal arteries is caused by interaction between glycoxidation and complement activation and contributes to the progression of diabetic nephropathy.

Acrolein↗

PubMed2005

The natural history of chronic renal failure: results from an unselected, population-based, inception cohort in Sweden.

BACKGROUND: Mortality rates in patients with chronic renal failure (CRF) are high both before and after start of renal replacement therapy (RRT). However, few studies of mortality and progression have been performed in an unselected CRF population. METHODS: We followed up a population-based inception cohort of 920 men and women aged 18 to 74 years who had CRF (serum creatinine level > 3.4 mg/dL [>300 micromol/L] for men and >2.8 mg/dL [>250 micromol/L] for women) for 55 to 79 months. Relationships between the outcomes (death and start of RRT) and independent variables under study (age, sex, primary renal disease, body mass index [BMI], and glomerular filtration rate [GFR] at entry) were explored by using Cox regression models. RESULTS: Seven hundred thirty-nine patients (80%) started RRT during the follow-up period. As expected, GFR at entry was clearly linked to the incidence of RRT (P < 0.0001). Age was related inversely to incidence of RRT (adjusted relative risk for patients > or =65 years relative to patients <45 years, 0.72; 95% confidence interval, 0.57 to 0.90). Men progressed to RRT more often than women (adjusted relative risk, 1.59; 95% confidence interval, 1.35 to 1.88). BMI was unrelated to RRT incidence. By the end of follow-up, 389 patients with CRF (42%) had died, 89 of them (10%) before the start of RRT. The most common primary cause of death was cardiovascular disease (37.5%). Characteristics significantly related to a greater mortality rate included older age, diagnoses of diabetic nephropathy and nephrosclerosis, and low BMI. CONCLUSION: Preuremic characteristics (age, sex, primary renal diagnosis, BMI, and GFR) are predictive of prognosis in unselected patients with CRF.

Adolescent↗

PubMed2006

Cardiovascular outcomes in the African American Study of Kidney Disease and Hypertension (AASK) Trial.

BACKGROUND: Patients with chronic kidney disease are at increased risk for cardiovascular (CV) events. METHODS: We randomly assigned 1,094 African Americans with hypertensive nephrosclerosis (glomerular filtration rate [GFR], 20 to 65 mL/min/1.73 m(2) [0.33 to 1.08 mL/s]) to initial antihypertensive treatment with either: (1) a beta-blocker, metoprolol; (2) an angiotensin-converting enzyme inhibitor, ramipril; or (3) a dihydropyridine calcium channel blocker, amlodipine, and either a usual-blood pressure (BP) or low-BP treatment goal. Using a design powered to detect renal outcome differences, we compared the effect of treatment on the CV event rate (cardiac death, myocardial infarction, stroke, and heart failure) during a mean follow-up period of 4.1 years and determined baseline factors that predict CV outcomes. RESULTS: Thirty-one patients died of CV disease (0.7%/patient-year), and 149 patients experienced at least 1 CV outcome (3.3%/patient-year). Overall, 202 CV events (4.5%/patient-year) occurred. The CV outcome rate was not related significantly to randomized interventions. In multivariable analyses, 7 baseline risk factors remained independently associated with increased risk for the CV composite outcome after controlling for age, sex, baseline GFR, and baseline proteinuria group: pulse pressure, duration of hypertension, abnormal electrocardiogram result, non-high-density lipoprotein cholesterol level, serum urea nitrogen level, urine protein-creatinine ratio, urine sodium-potassium ratio, and annual income less than 15,000 dollars. CONCLUSION: Neither randomized class of antihypertensive therapy nor BP level had a significant effect on the occurrence of CV events, possibly because of limited power. However, this analysis identifies unique and potentially modifiable CV risk factors in this high-risk cohort.

Adolescent↗

PubMed1983

Remission of essential hypertension after renal transplantation.

Six patients in whom "essential hypertension" led to nephrosclerosis and kidney failure received kidney transplants from normotensive donors. After an average follow-up of 4.5 years, all were normotensive and had evidence of reversal of hypertensive damage to the heart and retinal vessels. These six patients, all of whom were black, and six control subjects matched for age, sex, and race were admitted to the General Clinical Research Center for 11 days for observation of their blood pressure and their responses to salt deprivation and salt loading. Mean arterial pressure (+/- S.E.M.) among the patients who had previously had essential hypertension was similar to that of the normal controls (92 +/- 1.9 vs. 94 +/- 3.9; P not significant), and both groups had similar responses to salt deprivation and salt loading. Thus, essential hypertension in human beings is shown to be similar to the hypertension seen in spontaneously hypertensive rats in that both can be corrected by transplantation of a kidney from a normotensive donor. This observation supports the concept of the primary of the kidney in causing essential hypertension.

Adult↗

PubMed1976

Late somatic effects in syngeneic radiation chimaeras. III. Observations on animals repopulated with irradiated marrow.

Lethally-irradiated mice received a graft of bone-marrow cells obtained from intact syngeneic animals or from donors pre-irradiated with 200 or 400 rad. The numbers of haemopoietic cells injected were sufficient to give a high percentage of recipients which survived short-term bone-marrow failure. Epidemiological and pathological observations on long-term surviving animals showed an increased incidence of nephrosclerosis and of systemic or solid tumours following different relationships with the radiation dose given to the cells. These data are discussed within the framework of an experimental model system which might allow estimates of incidence of some neoplastic diseases according to cellular hypotheses of tumour induction.

Animals↗

PubMed1995

Calcium channel blockers and renal dysfunction in arterial hypertension.

Beside effective systemic blood pressure control, calcium channel blockers exert several effects on glomerular haemodynamics (namely, preglomerular vasodilatation at the early stage of the hypertensive process) and on cellular mechanisms of glomerular sclerosis (namely, inhibition of mesangial mechanisms of growth) that may provide a renal protective effect in patients with essential hypertension and, in turn, may prevent or attenuate the development of nephrosclerosis (Table 3). However, up to now, there have been relatively few attempts to corroborate this assumption in clinical practice. Furthermore, more clinical studies have been conducted with the dihydropiridine class of calcium channel blockers. Thus, prospective, long-term ongoing studies will help to delineate the long-range consequences of the renal actions of the different class of calcium channel blockers in essential hypertension.

Calcium Channel Blockers↗

PubMed1993

Chronic renal failure in India.

In a series of 2028 patients with chronic renal failure, the diseases leading to renal failure, the presence or absence of reversible factors and their nature, and the rate of decline of renal function of the most common conditions have been described and analysed. Seven diseases: chronic interstitial nephritis (27.85%), diabetic nephropathy (26.76%), chronic glomerulonephritis (18.20%), benign nephrosclerosis (10.06%), chronic pyelonephritis (7.29%), focal glomerulosclerosis (3.20%), and autosomal dominant polycystic disease of the kidneys (2.07%), accounted for 95.43% of all the patients. These diseases were studied in greater detail and the results are presented here. It was found that there was a great variation in the rate of decline of renal function in the different groups, with chronic glomerulonephritis and focal glomerular sclerosis progressing most rapidly, diabetic nephropathy slightly slower, and the others at a less alarming pace. However, once serum creatinine had reached 177 mumol/l there was an inexorable decline in renal function and the end stage was reached in almost all patients.

Adult↗

PubMedDate not supplied

Central retinal vein occlusion associated with hemodialysis.

Central retinal vein occlusion (CRVO) occurred in 3 of 15 maintenance hemodialysis patients over a two-week period. There have been no previous reports of this ophthalmologic catastrophe observed in the dialysis setting. Lupus nephritis, Henoch-Schönlein purpura and nephrosclerosis constituted the patients' major underlying diseases. Moderate hypertension was also present. Impaired vision of the left eye noted 24 to 36 hours following dialysis was the presenting symptom in all cases. Findings included decreased visual acuity, retinal vein engorgement, hemorrhage, and disc edema. All three patients subsequently lost the vision in their left eye (two received anticoagulation therapy). With the exception of hypertension, there were no known underlying predisposing conditions present. Although we are unable to offer a definite explanation for these unusual cases of CRVO, we feel a hypercoagulable state may have been responsible. Because our three cases occurred during a two-week period, some transient unidentified procoagulant factor associated with hemodialysis could have been present.

Adolescent↗

PubMed1999

The kidney as part of the cardiovascular system.

Renal vascular damage caused by arterial hypertension brings about changes in the systemic vascular function and structure. Nephrosclerosis appears to run in parallel with systemic atherosclerosis, accounting for the increased cardiovascular morbidity and mortality in hypertensive patients. Parameters indicating a change in renal function (increased serum creatinine concentration, proteinuria, and microalbuminuria) are independent predictors of increased cardiovascular morbidity and mortality and must therefore be considered in the classification of cardiovascular risk in hypertensive patients.

Albuminuria↗

PubMed1994

Pathophysiology of progressive renal failure.

Progressive renal failure is conditioned by a number of factors, including type of renal disease, sex, level of arterial pressure, insulin deficiency and/or hyperglycemia in diabetes mellitus, and dietary protein intake. Elevated arterial pressure may cause a progressive renal disease, hypertensive nephrosclerosis, and accelerate the rate of progression of all other chronic renal disease. Hypertension contributes to progressive renal failure by inducing myointimal hyperplasia of arcuate and afferent arterioles, causing glomerular ischemia, and by increasing pressure in the glomerular capillaries. The latter leads to hyperfiltration of protein, increased mesangial ingestion of protein, and glomerular sclerosis. Increased glomerular pressure may also be induced by protein feeding, insulin deficiency and hyperglycemia, especially in the presence of reduced nephron number. Thus at least one common mechanism underlies the effect of hypertension, protein feeding, and diabetes on the progression of chronic renal disease.

Humans↗

PubMed1997

Renal implications of arterial hypertension.

Renal vascular damage caused by arterial hypertension participates in alterations of the systemic vascular function and structure. Nephrosclerosis seems to run in parallel with the systemic atherosclerosis that accounts for the increased cardiovascular morbidity and mortality seen in hypertensive patients. Parameters indicating the existence of an alteration in renal function (increased serum creatinine, proteinuria and microalbuminuria) are independent predictors for an increased cardiovascular morbidity and mortality. Hence, parameters of renal function must be considered in any stratification of cardiovascular risk in hypertensive patients.

Albuminuria↗

PubMed1975

Differential count of urinary leucocytes and renal epithelial cells by phase contrast microscopy.

A total of 291 urine sediments from 255 patients with various renal or urinary tract diseases have been studied by phase contrast microscopy. Based upon morphological criteria, leucocytes were distinguished from renal epithelial cells and the white blood cells were classified either as mononuclear or polynuclear in 179 patients. The percentage of the different cell types varied considerably between and within the different diseases. The median values for polynuclear granulocytes were higher than 90% in bacterial renal or urinary tract disease and in polycystic kidney disease. In interstitial nephritis, nephrosclerosis and in renal transplanted patients the percentage of polynuclear granulocytes was somewhat lower, 76-85%. In diabetes, amyloidosis, tubular nephrosis (necrosis) glomerulonephritis, lupus nephritis and endemic benign nephropathy there were 14-66% polynuclear granulocytes. 29-33% mononuclear leucocytes were found in lupus nephritis and endemic benign nephropathy. The greatest proportion of renal epithelial cells was found in endemic benign nephropathy, namely 49%. 36% renal epithelial cells were found in tubular nephrosis (necrosis) and in glomerulonephritis. The technique is rapid and inexpensive. It facilitates differential diagnostics of urinary tract disease with pyuria.

Amyloidosis↗

PubMedDate not supplied

Sodium balance and plasma renin activity during the development of two-kidney Goldblatt hypertension in rats.

1. In two experiments severe hypertension (systolic blood pressure 180 mmHg) was induced in rats by constricting one renal artery with a silver clip (two-kidney, one clip hypertension; 2KIC). Blood pressure, plasma renin activity (PRA) and body weight were measured for 35 days after clipping. Plasma sodium concentration and carcass sodium content were measured at the conclusion of the experiment. To determine the relationship between sodium intake, PRA and the development of severe hypertension, half of the rats were given a normal diet and water to drink; the other half were given a low sodium diet and 0.9% saline to drink. 2. In both experiments, two patterns of responses were observed. Group (1) had reduced growth rate, and marked elevation of PRA. Some, but not all of these animals had histological evidence of malignant nephrosclerosis in the untouched kidney. In the other group (11), weight gain was normal and PRA was normal or only slightly elevated. 3. Group 1 animals drinking saline, had raised carcass sodium levels, whereas those drinking water had no increase in carcass sodium. 4. The results confirm that hypertension in the 2KIC model is not always associated with a raised PRA. 5. The coexistence of a raised PRA and increased total body sodium suggests that the PRA does not rise as a result of sodium depletion in this model.

Animals↗