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PubMed1995

Expression of vascular endothelial growth factor in renal vascular disease and renal allografts.

Vascular endothelial growth factor (VEGF) is a dimeric glycoprotein that exerts a proliferative effect specifically on endothelial cells. VEGF can increase vascular permeability and collagenase activity, is chemotactic for monocytes, and may dilate blood vessels. It can be induced by phorbol ester and cAMP in both mesenchymal and epithelial cells. In vitro cell culture experiments suggest that VEGF is upregulated by oxygen deprivation. In this study we tested whether in vivo acute and/or chronic reduction of renal blood flow by vascular obstruction would result in increased expression of VEGF mRNA and protein. Three normal kidneys, five human kidneys with narrowing of preglomerular vessels by vascular rejection or by vasculitis, and eight kidneys with nephrosclerosis and/or diabetic nephropathy were examined. In situ hybridization with 35S-labelled riboprobes showed a pronounced expression of VEGF mRNA in acutely hypoxic proximal and distal tubules of both the cortex and medulla; VEGF protein was demonstrated in the epithelia of these tubules by immunohistochemistry. In kidneys with chronically reduced blood flow, the majority of atrophic tubules were negative for VEGF mRNA and protein, although interstitial cells expressed VEGF mRNA. In arcuate arteries showing intimal and adventitial fibrosis, some medial smooth muscle cells were positive for VEGF mRNA. In glomeruli with segmental sclerosis, viable podocytes showed a prominent signal for VEGF mRNA. Mesangial cells did not express VEGF in the cases studied. It is possible that hypoxia itself led to the upregulation of VEGF in tubular epithelia and vascular smooth muscle cells. The vasodilatory and permeability-promoting effects of the endothelial growth factor produced by damaged tubular epithelia may constitute a mechanism to alleviate a decrease in blood flow and substrate availability and to re-establish vascular integrity.

Acute Disease↗

PubMed1994

Rarity of hypertensive stigmata in aging renocortical arteries of Bolivians.

Numerous reports have accumulated from around the world throughout the twentieth century of small, remote, self-sufficient populations that do not show a rise of blood pressure with age. Knowing that renocortical arteriosclerosis, a defining feature of hypertensive nephrosclerosis, is a close commensurate of blood pressure, it can be predicted that the elderly members of such populations should fail to show arteriosclerosis of hypertensive degree in the renal cortex. Emigrants from such populations sometimes come to medical attention in places like La Paz, Bolivia. Reported here are findings in autopsy samples of kidney tissue examined in La Paz. These samples have revealed remarkably little renovasculopathy at all ages up to 80 years, a phenomenon that has not previously been observed. Because of these findings, it can now be seen as biologically possible for a whole population of elderly persons to avoid renovasculopathy of hypertensive degree, and by implication, perhaps never experience hypertensive cardiovascular disease.

Adolescent↗

PubMed1994

Accelerated hypertension and nephroangiosclerosis associated with antiphospholipid syndrome. Report of two cases and review of the literature.

We describe two patients with the primary antiphospholipid syndrome who presented with severe hypertension. Renal biopsy specimen provided histologic evidence of intra-renal vascular disease with intravascular microthrombosis and nephrosclerosis, without feature of proliferative glomerulopathy. Accelerated hypertension and nephroangiosclerosis might indeed be one of the complications associated with anticardiolipin antibodies. The mechanism responsible might be the interaction of anticardiolipin antibodies, platelets and endothelial cell leading to microthrombi formation and increased local mitogenic activity that attract and stimulate neighbouring smooth muscle cell and fibroblast proliferation.

Adult↗

PubMed1999

Severe hypertensive sequelae in a child with Seckel syndrome (bird-like dwarfism).

We report a 19-year-old male with Seckel syndrome (bird-like dwarfism) who presents with malignant hypertension associated with hypertensive nephrosclerosis, dilated cardiomyopathy, and a ruptured cerebral artery aneurysm. Although end-organ injury due to chronic hypertension occurs frequently in adults, no previous reports of renal insufficiency due to hypertension exist in children or adolescents. We speculate that this patient may have been particularly prone to hypertensive end-organ injury due to his extreme short stature.

Adult↗

PubMed2006

Hypertension and kidney disease: a deadly connection.

Kidney disease may be the cause or a consequence of hypertension. Hypertension affects 25% of the adult population in the United States. Similarly, chronic kidney disease (CKD) and end-stage renal disease (ESRD) have been steadily increasing in incidence because of the increasing age of the US population and rise in the incidence of risk factors, including hypertension. Substantial evidence supports the notion that elevated blood pressure is the most significant risk factor for the development of CKD. Microalbuminuria has been shown to be the early marker of hypertensive renal disease. Furthermore, therapy to reduce microalbuminuria was associated with delay in the progression of renal disease. Black Americans are at higher risk for developing hypertensive nephrosclerosis than whites. Hypertension is a major risk factor for cardiovascular events in patients with CKD and ESRD and those who have undergone renal transplantation. Studies have documented that elevated serum creatinine and CKD are risk factors for a cardiovascular event. Tight blood pressure control has been shown to reduce microalbuminuria and proteinuria and to delay progression of renal disease. Tailoring the choice of antihypertensive medication to the clinical setting to achieve a blood pressure goal is critical in reducing complications from this deadly connection.

Black or African American↗

PubMed2006

Lessons from the African-American Study of Kidney Disease and Hypertension: an update.

Hypertension is the second leading attributable cause of end-stage renal disease in the United States today. The African-American Study of Kidney Disease and Hypertension was a randomized, double-blind, controlled trial designed to determine whether strict blood pressure (BP) control, angiotensin-converting enzyme inhibitor (ACEI)-based, or calcium channel blocker (CCB)-based regimens were superior to less strict BP control and beta-blocker (BB)-based regimens, respectively. The study enrolled 1093 African Americans with hypertensive nephrosclerosis and followed them for 4 years with repeated direct measurement of glomerular filtration rate (GFR) and monitoring of end points, including rapid decline in GFR, end-stage kidney disease, and death. From this landmark study, we learned that strict BP control is achievable in this study population, but it did not slow progression of kidney disease, and we learned that an ACEI-based therapy was superior to either a BB- or CCB-based regimen. In addition, we learned that proteinuria is the most important predictor of progression of kidney disease; ACEI and CCB have differential effects on proteinuria; and a CCB-based regimen combined with strict BP control may be the next best choice to an ACEI-based regimen in this population.

Adrenergic beta-Antagonists↗

PubMed2004

Demographic, pathologic, and toxicological profiles of 127 decedents testing positive for ephedrine alkaloids.

The relative toxicity of ephedra-containing dietary supplements is disputed. In order to ascertain the magnitude of the problem, we reviewed all autopsies in our Medical Examiner's jurisdiction, from 1994 to 2001, where ephedrine or any its isomers (E+) were detected. Toxicology testing results were tabulated and anatomic findings in E+ cases were compared to those in a control group of drug-free trauma victims. Of 127 E+ cases identified, 33 were due to trauma. Decedents were mostly male (80.3%) and mostly Caucasian (59%). Blood ephedrine concentrations were <0.49 mg/l in 50% of the cases, range 0.07-11.73 mg/l in trauma victims, and 0.02-12.35 mg/l in non-trauma cases. Norephedrine (NE) was present in the blood of 22.8% (mean of 1.81 mg/l, S.D.=3.14 mg/l) and in the urine of 36.2% (mean of 15.6 mg/l, S.D.=21.50mg/l). Pseudoephedrine (PE) was present in the blood of 6.3% (8/127). More than 88% (113/127) of the decedents also tested positive for other drugs, the most common being cocaine (or its metabolites) and morphine. The most frequent pathologic diagnoses were hepatic steatosis (27/127) and nephrosclerosis (22/127). Left ventricular hypertrophy was common, and coronary artery disease (CAD) detected in nearly one third of the cases. The most common findings in E+ deaths are those generally associated with chronic stimulant abuse, and abuse of other drugs was common in those with CAD. There were no cases of heat stroke or rhabdomyolysis. In most cases, norephedrine was not detected, suggesting it plays no role in ephedrine toxicity.

Adolescent↗

PubMed2005

Continuous inhibition of the renin-angiotensin system and protection from hypertensive end-organ damage by brief treatment with angiotensin II type 1 receptor blocker in stroke-prone spontaneously hypertensive rats.

To investigate the short-term blockade of angiotensin II type 1 (AT1) receptor at the prehypertensive stage and its effects on hypertensive sequelae after maturation, we administered AT1 receptor blocker (ARB, 1 mg/kg/day) to male stroke-prone spontaneously hypertensive rats (SHRSP) from 5 to 10 weeks of age. Although blood pressure in the treated group was significantly lower than in the control group at 10 weeks of age, it gradually increased within 2-3 weeks and reached approximately 250 mm Hg at 17 weeks after cessation of the treatment (27 weeks of age), and reached parity with the control after 20 weeks of age. Nonetheless, hypertensive end-organ damage such as cerebral lesion, cardiac hypertrophy and nephrosclerosis were markedly suppressed in the treated group. Plasma renin activity (PRA), plasma angiotensin II (AII) levels and cerebral angiotensin-converting enzyme (ACE) activity were also significantly lower in the treated group than in the control group, indicating continuous suppression of the circulating and local renin-angiotensin system (RAS). In the brain, intercellular adhesion molecule-1 (ICAM-1) mRNA expression was significantly lower in the cerebral cortex of the treated group than in the control group, while AT1 receptor expression was similar. Such beneficial effects by ARB treatment were not found in the hydralazine-treated group, even though blood pressure changes were similar in both groups. These results demonstrated that early and transient treatment by ARB effective for the prevention of hypertensive end-organ damage. This may be due to the low concentration of plasma angiotensin II by continuous inhibition of RAS even after maturation.

Angiotensin II↗

PubMed1987

Renal parenchymal involvement in essential hypertension.

This article has reviewed the involvement of the kidney as a target organ of essential hypertension. Since Bright first made the association of renal disease and hypertension in 1836, the nature of this relationship has been debated. Although there is evidence implicating abnormalities of renal function in the pathogenesis of essential hypertension, hypertension frequently precedes histologic evidence of alterations in renal structure. Nephrosclerosis, or hardening of the kidney, is the term used to describe the histologic changes occurring in the kidney as the result of hypertension. It can be though of as an acceleration of the normal aging process of the renal vasculature. Glomerular and tubular changes have been traditionally thought to be ischemic in origin. Experimental evidence supports the notion that, as renal function is lost, intraglomerular hypertension develops and may be responsible for additional nephron loss in hypertension. This idea may have therapeutic implications for hypertensive patients with renal insufficiency in that agents that reduce both systemic and intraglomerular pressure may be preferable. Hemodynamically, early hypertension is often characterized by normal peripheral and renal vascular resistance and an increased cardiac output. In established hypertension, cardiac output is usually normal, and peripheral and renal vascular resistances are increased. Renal blood flow is reduced, glomerular filtration rate is maintained, and the filtration fraction rises. In the absence of an accelerated malignant phase, renal failure is uncommon in essential hypertension. Males and blacks are most sensitive to the vascular damage of essential hypertension. Essential hypertension remains an important cause of end-stage renal disease, especially in blacks. Atherosclerotic obstruction of the renal arteries may be a more common cause of renal failure in patients with essential hypertension than has been previously recognized. There are few sensitive markers of early renal involvement in essential hypertension. Several studies of sensitive markers are promising and may detect patients who are prone to renal injury and deserve more aggressive treatment. Malignant hypertension is characterized pathologically by vascular changes of proliferative endarteritis and fibrinoid necrosis. Fortunately, its frequency is decreasing because of early identification and effective treatment of essential hypertension. Effective treatment of severe and malignant hypertension clearly leads to stabilization (and occasionally improvement) of renal function.(ABSTRACT TRUNCATED AT 400 WORDS)

Hemodynamics↗

PubMed1985

Preferential effectiveness of cyclosporin in patients receiving kidney transplants after glomerulonephritis.

Glomerulonephritis patients transplanted with cadaver kidneys had a significantly higher one-year graft survival when immunosuppressed with cyclosporin rather than standard therapy (80% versus 59%, p less than 10(-5]. For nephrosclerosis patients the corresponding rates were 70% and 59% (p greater than 0.05); and in those with antecedent diabetes mellitus, polycystic kidney, and pyelonephritis the differences were negligible. In glomerulonephritis patients, but not in the other groups, cyclosporin was additive to the effect of transfusions and of HLA-A, B and HLA-Dr matching.

Cyclosporins↗

PubMed2000

Gender difference in the mean age at the induction of hemodialysis in patients with autosomal dominant polycystic kidney disease.

Male patients with autosomal dominant polycystic kidney disease (ADPKD) begin hemodialysis earlier than female patients. The rate of progression of many other renal diseases is also faster in men than women. In this study, gender difference in ADPKD was compared with that in other diseases, such as chronic glomerulonephritis, diabetic nephropathy, and nephrosclerosis, using the data obtained from an annual statistical survey of the Japanese Society for Dialysis Therapy. The male-female ratio in ADPKD (n = 8,176) was 1.17:1 and closer to 1.0:1 than the other diseases. Men with ADPKD started hemodialysis therapy 1.3 years earlier than women (male age, 55.9 +/- 12.4 years versus female age, 57.2 +/- 11.5 years), and the age difference was less than that in other diseases. These results suggest that the prognosis in women with ADPKD is relatively worse than that in men with ADPKD or that women are not well protected against the progression of this disease compared with other renal diseases. In conclusion, men with ADPKD are introduced to hemodialysis therapy earlier than women; however, the age difference was small compared with other common renal diseases.

Adolescent↗

PubMed2003

Sirolimus-induced thrombotic microangiopathy in a renal transplant recipient.

A rare but well-documented serious adverse reaction to the administration of the calcineurin inhibitors tacrolimus and cyclosporine in renal transplant recipients is the development of medication-induced thrombotic microangiopathy. The recently introduced immunosuppressive medication sirolimus has a very similar molecular structure to tacrolimus and also binds to the same intracellular proteins. Despite these similarities with tacrolimus, sirolimus has a different side-effect profile and reportedly lacks documented specific renal toxicity. This is a case report of the isolated administration of sirolimus without a concomitant calcineurin inhibitor being associated with the development of renal transplant biopsy-proven thrombotic microangiopathy. The patient is a 47-year-old African-American woman whose primary cause of renal failure was not thrombotic micrangiopathy, and she received a 5-antigen mismatched cadaveric renal transplant. Because of preexisting nephrosclerosis in the renal transplant, this patient was never administered a calcineurin inhibitor but was always maintained on sirolimus. With recent animal data showing that sirolmus can be nephrotoxic in a renal ischemic-reperfusion model (similar to what happens with a renal transplant), the authors speculate on a mechanism for this adverse reaction.

Adult↗

PubMed1983

Relationship of creatinine clearance to orthoiodohippurate measured effective renal plasma flow.

Effective renal plasma flow (ERPF) was measured utilizing 1-131 orthoiodohippurate (OIH). The OIH ERPF was correlated in 50 patients with routine 24-hour urine creatinine clearance measurements and with a formula predicting creatinine clearance based on age, weight, and serum creatinine (formula creatinine clearance). The filtration fraction (routine creatinine clearance/OIH ERPF) in 38 patients with hypertensive nephrosclerosis, tubulointerstitial renal disease, or normal renal function were compared. Filtration fractions in the three groups tested were not statistically different. ERPF had a correlation coefficient of 0.62 with routine creatinine clearance and 0.72 with formula creatinine clearance. Thus, OIH ERPF correlates with creatinine clearance measurements but cannot be used to replace creatinine clearance as a method of evaluating renal function. The reasons for the lack of a stronger positive correlation between ERPF and glomerular filtration rate (GFR) remain to be elucidated.

Adult↗

PubMed1999

Exacerbation of glomerulonephritis in subjects with chronic hepatitis C virus infection after interferon therapy.

We previously reported the glomerular deposition of hepatitis C virus (HCV) core antigen (Ag) in HCV-related nephropathy. In this study, we analyzed 23 HCV-positive subjects with exacerbation of proteinuria and/or hematuria during interferon (IFN) therapy and measured urinary protein selectivity. We also examined the involvement of HCV-related Ag using anti-HCV core (capside) Ag murine monoclonal antibody (Ab) and anti-core2 rabbit polyclonal Abs in nine subjects. Of 17 subjects, 13 (78%) showed low selective proteinuria. We found mesangial proliferative glomerulonephritis in 9 subjects, membranoproliferative glomerulonephritis in 1 subject, and nephrosclerosis in 1 subject. Immunofluorescence study showed the glomerular deposition of immunoglobulin G (IgG) or IgA and complements in all 9 subjects examined. Trace amounts only of HCV core Ag were detected along the glomerular capillary wall in 3 of 9 subjects (33%). Electron microscopy showed subendothelial or mesangial electron-dense deposits and also foot process effacement (20% to 72.5% of glomerular capillary walls) in all subjects and endothelial swelling in 4 subjects. In conclusion, IFN therapy for HCV may exacerbate the underlying glomerulopathies, unrelated to HCV Ags, through direct or indirect effects on glomerular endothelial and epithelial cells. Physicians should carefully distinguish HCV-related nephropathy from other glomerular diseases when they administer IFN therapy to HCV-positive subjects.

Adult↗

PubMed1995

Surgical management of dialysis-dependent ischemic nephropathy.

PURPOSE: This retrospective review describes surgical management of dialysis-dependent ischemic nephropathy. METHODS: From February 1987 through September 1993, 340 patients underwent operative renal artery (RA) reconstruction at our center. A subgroup of 20 patients (6 women; 14 men; mean age 66 years) dependent on hemodialysis immediately before RA repair form the basis of this report. Glomerular filtration rates (EGFR) were estimated from at least three serum creatinine measurements obtained 26 weeks before and after operation. A linear regression model was used to estimate the mean rate of change of EGFR before and after RA repair. Comparative analysis of kidney status and change in EGFR were performed. The influence of function response on follow-up survival was determined by the product-limit method. RESULTS: Hemodialysis was discontinued in 16 of 20 patients (80%). For these 16 patients, postoperative EGFR ranged from 9.0 to 56.1 ml/min/1.73 m2 (mean 32.4 ml/min/1.73 m2). Two of 16 patients resumed hemodialysis 4 and 6 months after surgery. Discontinuation of dialysis was more likely after bilateral or complete RA repair (15 of 16 patients) versus unilateral repair (one of four patients; p = 0.01). Permanent discontinuation of dialysis was associated with a rapid preoperative rate of decline in EGFR (mean slope log(e) EGFR: -0.1393 +/- 0.0340 without dialysis; -0.0188 +/- 0.0464 with dialysis; p = 0.04, but NS after controlling for multiple comparisons). Immediate increase in EGFR after operation was inversely correlated with the severity of nephrosclerosis (rank correlation: -0.57; 95% confidence interval [-0.83, -0.10]). Follow-up death was associated with dialysis dependence; two deaths occurred among 14 patients not receiving dialysis, whereas five of six patients dependent on dialysis died (p < 0.01). CONCLUSION: Surgical correction of ischemic nephropathy can retrieve renal function in selected patients dependent on dialysis characterized by a rapid decline in preoperative EGFR in combination with global renal ischemia treated by complete or bilateral renal revascularization. After RA repair, discontinuation of dialysis may be associated with improved survival rates when compared with continued dialysis dependence.

Aged↗

PubMed2005

Cardiovascular risk in patients with mild renal insufficiency: implications for the use of ACE inhibitors.

We review the evidence linking mild renal insufficiency (MRI) with increased cardiovascular risk. MRI is associated with a number of cardiovascular risk factors, including nighttime hypertension, and increased levels of lipoprotein (a), homocysteine, asymmetric dimethyl-arginine, and inflammation and insulin resistance markers and mediators. Epidemiologic evidence associates coronary artery disease and nephrosclerosis, a frequent cause of early renal insufficiency in the elderly. In a middle-aged general population MRI was found in 8% of women and 9% of men, but was not associated with cardiovascular disease. Nonetheless, in a representative sample of middle-aged British men the risk of stroke was 60% higher for the sub-group with MRI: in people at high cardiovascular risk (mostly coronary disease), the HOPE study found a 2-fold (unadjusted) or 1.4-fold (adjusted) higher incidence of cardiovascular outcomes with MRI. The combined incidence of cardiovascular death, myocardial infarction and stroke increased with the level of serum creatinine. Several studies have examined the cardiovascular risk associated with MRI in hypertension. In HDFP, as in HOPE, cardiovascular mortality increased with serum creatinine (five-fold difference in cardiovascular mortality between the lowest and the highest creatinine strata). The risk associated with renal insufficiency was independent of other classic cardiovascular risk factors. Two trials of hypertensives with low risk (HOT and a small Italian trial) found that cardiovascular outcomes approximately doubled in subjects with MRI. Another study (MRFIT) found that it was not baseline creatinine, but its increase on follow-up that predicted future cardiovascular disease. These observational data suggest that regardless of etiology MRI is a strong predictor of cardiovascular disease and is found in 10% of populations at low cardiovascular risk and in up to 30% of those at high risk. No prospective therapeutic trials aimed at reducing the cardiovascular burden in people with MRI are available. Subgroup analyses of the HOPE study indicate that angiotensin-converting enzyme (ACE) inhibition with ramipril is beneficial and does not increase the risk of such side effects as acute renal failure or hyperkalemia. Thus the frequent practice of withholding ACE inhibitors from patients with mild renal insufficiency is unwarranted, especially since MRI identifies a group at high risk that appears to benefit most from treatment. Moreover, there is evidence that ACE inhibitors improve renal outcomes in renal insufficiency. Prospective studies should test the predictive power of early renal insufficiency for cardiovascular disease and prognosis with various therapeutic options.

Age Factors↗

PubMed1984

Renal pathology in end-stage renal disease associated with paraplegia.

In the present study we report the renal pathological findings from autopsy material along with relevant clinical data on 21 spinal cord injury patients with end-stage renal disease (SCI-ESRD) treated with maintenance haemodialysis. These data are compared with the relevant clinical and post-mortem findings on 43 ambulatory dialysis patients who expired during the same time period. The SCI-ESRD patients exhibited markedly different clinical and renal histopathological data when compared to the ambulatory--ESRD group. Chronic pyelonephritis and amyloidosis dominated the findings and were the major causes of renal insufficiency. Acute pyelonephritis, papillary necrosis, calculous disease, pyonephrosis and perinephric abscess formation were also more frequently present in the SCI-ESRD patients. Hypertension and nephrosclerosis, which were common findings in the ambulatory--ESRD patients were comparatively rare in the SCI-ESRD patients. In addition, the incidence of acquired cystic disease (ACD) was considerably less in the SCI-ESRD group. Although the reasons for these findings are not entirely clear several possible explanations are given. Infection with gram negative sepsis was the predominant cause of death in the SCI-ESRD patients, while death secondary to cardiovascular disease predominated in the ambulatory-ESRD group. Furthermore, the urinary tract and infected decubitus ulcers were determined to be the major source for sepsis in the SCI patients. From these findings it would follow that more effective prevention and control of these infections would result in not only a lower incidence of renal failure but also a substantially reduced morbidity and mortality in chronic SCI.

Adult↗

PubMed1998

Total body irradiation and cyclophosphamide is a conditioning regimen for unrelated bone marrow transplantation in a patient with chronic myelogenous leukemia and renal failure on hemodialysis.

Five years after the diagnosis of Ph chromosome-positive chronic myeloid leukemia (CML) a 31-year-old patient developed malignant nephrosclerosis with renal failure. He then underwent an allogeneic unrelated BMT in first chronic phase CML. The preparative regimen consisted of fractionated total body irradiation (TBI) and cyclophosphamide (CY). We studied the pharmacokinetics of cyclophosphamide on hemodialysis and compared clinical parameters including time to engraftment and toxicity with parameters of a patient with normal renal function who also received an unrelated marrow as treatment for CML in first chronic phase. Our results suggest that TBI/CY is a suitable conditioning regimen for allogeneic transplantation in patients with hematological malignancy and renal failure on hemodialysis.

Adult↗