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PubMed2000

Aldosterone modulates plasminogen activator inhibitor-1 and glomerulosclerosis in vivo.

BACKGROUND: Aldosterone promotes nephrosclerosis in several rat models, whereas aldosterone receptor antagonism blunts the effect of activation of the renin-angiotensin-aldosterone system (RAAS) on nephrosclerosis, independent of effects on blood pressure. Based on recent findings linking activation of the RAAS with impaired fibrinolytic balance, we hypothesized that aldosterone induces sclerosis through effects on plasminogen activator inhibitor-1 (PAI-1), the major physiological inhibitor of plasminogen activation. METHODS: We examined the effect of aldosterone antagonism on the development of sclerosis and on renal PAI-1 expression following radiation injury in the rat. Following a single dose of 12 Gy to the kidneys, male Sprague-Dawley rats were treated with placebo, the aldosterone antagonist spironolactone (4.5 mg/day by time-release subcutaneous pellet), the angiotensin type 1 receptor antagonist L158-809 (AT1RA; 80 mg/L drinking water), or combined spironolactone and AT1RA. RESULTS: Rats treated with placebo developed significant proteinuria and nephrosclerosis 12 weeks following radiation associated with hypertension. Kidney PAI-1 mRNA expression was increased eightfold (P < 0.001 vs. nonradiated controls). Spironolactone alone had no effect on blood pressure (systolic blood pressure 149.0 +/- 5.4 mm Hg) compared with placebo (151.6 +/- 11.2 mm Hg, P = NS), whereas AT1RA alone (107.7 +/- 8.9 mm Hg, P = 0.013 vs. placebo) or in combination therapy (102.1 +/- 6.2 mm Hg, P = 0.001 vs. placebo) lowered blood pressure. Both the AT1RA and spironolactone decreased proteinuria following radiation (P < 0.001 vs. placebo for either drug), and the combination of AT1RA + spironolactone had a greater effect on proteinuria than spironolactone alone (P = 0.003). Aldosterone antagonism significantly decreased (P = 0.016 vs. placebo) and AT1RA virtually abolished (P = 0.001 vs. placebo) the development of sclerosis. Spironolactone significantly decreased PAI-1 mRNA expression in the kidneys of radiated animals (PAI-1 mRNA/GAPDH ratio 0.39 +/- 0.13 vs. placebo 0.84 +/- 0.05, P = 0.006), and there was a significant correlation between the degree of sclerosis and the level of PAI-1 immunostaining within individual rats (R2 = 0.97, P < 0.0001). CONCLUSION: This study is, to our knowledge, the first to demonstrate that aldosterone regulates PAI-1 expression in vivo, and supports the hypothesis that aldosterone induces renal injury through its effects on PAI-1 expression.

Aldosterone↗

PubMed2002

Higher urinary IgM excretion in type 2 diabetic nephropathy compared to type 1 diabetic nephropathy.

BACKGROUND: Proteinuria, due to impairment of the charge- and/or size selectivity of the glomerular capillary wall (GCW) is the earliest clinical evidence of diabetic nephropathy (DN). To study the pathophysiological differences between patients with DN in type 1 diabetes mellitus (type 1 DN) and type 2 diabetes mellitus (type 2 DN), we compared the patterns of urinary proteins of different size and charge in the two entities of diabetic kidney disease. METHODS: Urine concentrations of albumin, IgG2, IgG4 and IgM were assessed in 22 (15 males and 7 females) patients with type 1 DN, and in 20 (18 males and 2 females) patients with type 2 DN. Comparisons with one control group of 13 (12 males and one female) patients with nephrosclerosis due to systemic hypertension and a second control group of 16 (14 males and 2 females) healthy controls were made. RESULTS: The urine excretion of IgG2 and IgM and the ratio of IgG2 to IgG4 (IgG2/IgG4), were significantly higher in type 2 DN compared to type 1 DN (P < 0.01). Patients with type 2 DN and patients with nephrosclerosis had significantly higher urine excretion of IgG and IgM compared to the age-matched healthy subjects (P < 0.001). The IgG2/IgG4 ratio was higher in type 2 DN compared to nephrosclerosis and healthy controls (P < 0.01). CONCLUSION: The increased urine excretion of IgG and IgM that accompanies albuminuria in type 2 DN suggests that the dominant pathophysiological mechanism of proteinuria in type 2 DN might be an alteration of the size selective properties of the glomerular capillary wall, including the occurrence of non-discriminatory "shunt pathways." The charge selective properties of the glomerular capillary wall seem to be intact in type 2 DN, as indicated by the high IgG2/IgG4 ratio. The mechanisms of proteinuria in type 1 DN seem to be merely a consequence of an impaired charge selectivity of the glomerular capillary wall.

Adult↗

PubMed1975

Renal vascular tone in essential and secondary hypertension: hemodynamic and angiographic responses to vasodilators.

The renal vascular response to graded doses of acetylcholine, dopamine and phentolamine, assessed by xenon washout and selective arteriography was used to define the relative contribution of fixed and reversible vascular abnormalities to increased renal vascular resistance in patients with essential or secondary hypertension. The increase in blood flow induced by acetylcholine and dopamine was blunted strikingly in patients with advanced nephrosclerosis, chronic pyelonephritis and polycystic kidney disease and was normal in the kidney contralateral to a significant renal artery stenosis. Conversely, the response to both was potentiated in 9 of 13 (69%) patients with mild essential hypertension. Equivalent potentiation of the response to acetylcholine was induced in normal subjects by increasing renal vascular tone pharmacologically with angiotensin. Phentolamine infused into the renal artery also increased renal blood flow significantly in 6 of 9 (67%) patients with mild essential hypertension, but in none of 15 normal subjects, over a dose reange that paralleled that for alpha-adrenergic blockade. Changes in the selective renal arteriogram were in excellent accord: potentiated response to acetylcholine, phentolamine or dopamine was associated with reversal of the small vessel abnormalities visualized in the arteriogram. The reduced blood flow response in advanced nephrosclerosis or parenchymal disease was associated with a reduced angiographic change during dilator infusion. The results suggest a quantitatively important, functional renal vascular abnormality--perhaps mediated by the sympathetic nervous system--in many patients with mild essential hypertension. Conversely the renal vascular abnormality associated with advanced nephrosclerosis or renal parenchymal disease is largely fixed and is probably due to organic changes.

Acetylcholine↗

PubMed1997

Regional renal nitric oxide release in stroke-prone spontaneously hypertensive rats.

Diminished nitric oxide (NO) production has been implicated in the pathogenesis of salt-sensitive hypertension. We questioned whether such a defect is responsible for the malignant hypertension and nephrosclerosis in stroke-prone spontaneously hypertensive rats (SHRSP) fed a high-salt/stroke-prone diet (S) versus a regular diet (R). NO release from 30-minute incubates of cortex and outer and inner medulla were studied in SHRSP at 10, 12, and 16 weeks of age on the S diet versus R diet. SHRSP-S (n=16) exhibited a marked age-dependent increase in NO release, especially in the cortex. Increases were only modest in SHRSP-R (n=21). At 16 weeks, cortical NO was 93+/-25 versus 6+/-1 pmol/mg tissue in SHRSP-S versus SHRSP-R (P<.001). Immunohistochemical staining increased mostly for neuronal, slightly for endothelial, and negligibly for inducible isoforms of NO synthase and was predominantly in the cortex of SHRSP-S versus SHRSP-R. Despite similar hypertension in SHRSP-S versus SHRSP-R (mean arterial pressure, 174+/-7 versus 177+/-2 mm Hg), malignant nephrosclerosis was seen only in SHRSP-S, affecting 22+/-6% of glomeruli and 23+/-4 vessels per 100 glomeruli by 16 weeks. N omega-nitro-L-arginine (15 mg/kg per day) in SHRSP-S (n=6) abrogated the increase in cortical NO but further augmented the hypertension and accelerated lesion development. Wistar-Kyoto rats at 16 weeks on the R diet (n=8) had NO levels similar to those of SHRSP-R, showed increased cortical NO to only 28+/-10 pmol/mg on the S diet (n=9) (P<.05 versus SHRSP-S), but remained normotensive and lesion-free. We conclude that hypertension and lesion development in SHRSP are not due to deficient renal NO. Accelerated onset of malignant nephrosclerosis by NO synthase inhibition suggests that NO is protective in these animals, mitigating the effects of hypertension and S diet on renal pathology.

Aging↗

PubMed1999

Role of aldosterone in renal vascular injury in stroke-prone hypertensive rats.

Stroke-prone spontaneously hypertensive rats (SHRSP) on 1% NaCl drinking solution and Stroke-Prone Rodent Diet develop severe hypertension and glomerular and vascular lesions characteristic of thrombotic microangiopathy seen in malignant nephrosclerosis. We recently reported that spironolactone, a mineralocorticoid receptor antagonist, markedly reduced proteinuria and malignant nephrosclerotic lesions in these animals. This observation, together with our previous findings that angiotensin-converting enzyme inhibitors prevent the development of vascular damage, suggests that mineralocorticoids, as part of the renin-angiotensin-aldosterone system, play a pathophysiological role in this model. In the present study, we examined whether chronic (2-week) infusion of aldosterone can reverse the renal vascular protective effects of captopril in SHRSP. SHRSP received vehicle (n=8); captopril alone (50 mg. kg-1. d-1, orally) (n=10); aldosterone infusion alone (40 microg. kg-1. d-1, SC) (n=7); or captopril and aldosterone at 20 (n=6) or 40 (n=7) microg. kg-1. d-1. Systolic blood pressure was markedly elevated in all groups. Vehicle- and aldosterone-infused SHRSP developed severe proteinuria and comparable degrees of renal injury (21+/-3% and 29+/-3%, respectively) manifested as thrombotic and proliferative lesions in the arterioles and glomeruli. Captopril treatment reduced plasma aldosterone levels concomitant with marked reductions in proteinuria and the absence of histologic lesions of malignant nephrosclerosis. Aldosterone substitution at 20 or 40 microg. kg-1. d-1 in captopril-treated SHRSP resulted in the development of severe renal lesions (16+/-3% and 21+/-2%, respectively) and proteinuria comparable with that observed in SHRSP given either aldosterone or vehicle alone. These findings support a major role for aldosterone in the development of malignant nephrosclerosis in saline-drinking SHRSP, independent of the effects of blood pressure.

Aldosterone↗

PubMed2001

Angiotensin type 1 receptor antagonism and ACE inhibition produce similar renoprotection in N(omega)-nitro-L>-arginine methyl ester/spontaneously hypertensive rats.

This study was conducted to determine potentially differential effects between an angiotensin II type 1 (AT(1)) receptor antagonist and an ACE inhibitor on systemic, renal, and glomerular hemodynamics and pathological changes in spontaneously hypertensive rats (SHR) with N(omega)-nitro-L>-arginine methyl ester (L-NAME)-exacerbated nephrosclerosis. The hemodynamic, renal micropuncture, and pathological studies were performed in 9 groups of 17-week-old male SHR treated as follows: group 1, controls (n=16); group 2, candesartan (10 mg/kg per day for 3 weeks) (n=7); group 3, enalapril (30 mg/kg per day for 3 weeks) (n=8); group 4, candesartan (5 mg/kg per day) plus enalapril (15 mg/kg per day for 3 weeks) (n=9); group 5, L-NAME (50 mg/L in drinking water for 3 weeks) (n=17); group 6, L-NAME (50 mg/L) plus candesartan (10 mg/kg per day for 3 weeks) (n=7); group 7, L-NAME (50 mg/L) for 3 weeks followed by candesartan (10 mg/kg per day) for another 3 weeks (n=8); group 8, L-NAME (50 mg/L) plus enalapril (30 mg/kg per day for 3 weeks) (n=7); and group 9, L-NAME (50 mg/L) plus enalapril (30 mg/kg per day) and the bradykinin antagonist icatibant (500 microg/kg SC per day via osmotic minipump for 3 weeks) (n=7). Both candesartan and enalapril similarly reduced mean arterial pressure and total peripheral resistance index. These changes were associated with significant decreases in afferent and efferent glomerular arteriolar resistances as well as glomerular capillary pressure. Histopathologically, the glomerular and arterial injury scores were decreased significantly, and left ventricular and aortic masses also were diminished significantly in all treated groups. L-NAME-induced urinary protein excretion was prevented by both candesartan and enalapril. Thus, both AT(1) receptor and ACE inhibition prevented and reversed the pathophysiological alterations of L-NAME-exacerbated nephrosclerosis in SHR. Itatibant only blunted the antihypertensive effects of enalapril but did not attenuate the beneficial effects of ACE inhibition on the L-NAME-induced nephrosclerosis. Thus, the AT(1) receptor antagonism and ACE inhibition have similar renal preventive effects, which most likely were achieved through reduction in the effects of angiotensin II, and ACE inhibition of bradykinin degradation demonstrated little evidence of renoprotection.

Adrenergic beta-Antagonists↗

PubMed1999

[Vascular mechanisms of renal fibrosis. Vasculonephropathies and arterial hypertension].

Nephrovasculopathies are an increasing cause of end-stage renal failure. Nephrosclerosis is a common finding in the hypertensive patient. However, genetic factors play a prominent role in its incidence. Nephrosclerosis is a common cause of early renal failure in blacks of African ancestry, as opposed to white Europeans, in whom hypertensive nephrosclerosis rarely and slowly leads to uremia. That primary hypertension is accompanied by arterionephrosclerosis and arteriolonephrosclerosis, by focal and segmental glomerulosclerosis leading to glomerular obsolescence and by interstitial fibrosis has been established for nearly a century. However, renal vascular lesions can be observed in animal models as well as in some humans, especially blacks, in the absence of, or preceding the onset of hypertension. This suggests that nephroangiosclerosis might stem from a genetic defect in the renal vascular bed, a defect closely associated with the hypertensive trait. Atherosclerotic renal artery stenosis is a major, potentially remediable cause of chronic renal failure, especially in whites. Its prevalence in the atherosclerotic population is in the order of 15 percent. This figure has obvious bearing in terms of health cost. Early diagnosis and treatment by angioplasty or surgery can preclude development to end-stage renal disease and maintenance hemodialysis, as renal atrophy due to chronic ischemia resulting from renal artery stenosis can be halted or partially reversed by revascularization before extensive fibrosis sets in. Finally, renal vascular lesions are commonly observed in the course of various nephropathies, even in the absence of hypertension. The relationship between fibrogenesis and these vascular lesions, which develop along with interstitial fibrosis and entail an unfavorable prognosis in various glomerulopathies, remains to be elucidated. This is especially the case for focal-segmental glomerulosclerosis, membranous glomerulopathy and IgA glomerulonephritis. The pathophysiology of renal fibrosis induced by ischemia is centered on increased generation of angiotensin II that is fibrogenic owing to interaction with endothelin 1, PDGF-BB and TGF-beta. These notions open perspectives toward pharmacologic means to retard or even prevent the development of such various ischemic conditions to end-stage renal failure.

Fibrosis↗

PubMed2004

[Incidence of chronic renal failure during 35 years at the Rijeka Clinical Hospital Center].

Chronic hemodialysis treatment in the world started in 1960. At that time, due to technical development and construction of arteriovenous shunt for repeated blood access for dialysis, it was possible to treat uremia. At the Department of Surgery, Rijeka Clinical Hospital, former Dr. Zdravko Kucić Hospital, first hemodialysis was performed in 1962, whereas regular chronic dialysis treatment started in 1966. On September 20, 1966, the first hemodialysis was done in a patient with chronic uremia. A week later, the next patient was admitted for therapy. The aim of the study was to analyze demographic and other data of all patients who started dialysis in the period between 1966 and 2001. There were 910 patients, 555 (60.9%) male and 355 (39.1%) female. In the first year, only two patients were treated with hemodialysis. Until 1970, the number of new patients was 4 or 5. From 1971 till 1984 between 10 and 19 new patients started dialysis every year, and from 1985 till 1990 their number ranged from 23 to 34 per year. Further increase in the number of treated patients was recorded in 1990 when 42 patients were dialyzed. In the following years until 2001 the figures were between 40 and 58, and in 2001 55 new patients were treated. In 1966, the mean age of patients undergoing this therapy was 29.5 years, and with time it increased to 40 in 1978. From 1989 on, the mean age rose to 50, and from 1998 to 60. In 2001, the mean patient age was 63.2 years. The primary renal diseases that led to uremia in the study population were glomerulonephritis (GN) in 256 (28.1%), pyelonephritis (PN) in 165 (18.1%), diabetes mellitus (DM) in 161 (17.7%), nephrosclerosis in 111 (12.2%), uremia after transplanted kidney rejection in 47 (5.2%), polycystosis in 40 (4.4%), lupus nephritis in 12 (1.3%), other causes in 89 (9.7%), and unknown cause in 24 (2.6%) patients. The distribution of primary renal disease during the observed period was as follows: from 1966 till 1979 the cause of uremia was GN in 88 (62%), PN in 30 (21.1%), DM in only 1, polycystosis in 3, post-transplant uremia in 7, lupus in 3, and other causes in 7 patients. From 1980 to 1989, GN was the cause of uremia in 67 (31.6%), PN in 45 (21.2%), DM in 22 (10.4%), nephrosclerosis in 26 (12.3%), polycystosis in 11 (5.2%), post-transplantation uremia in 12 (5.7%), lupus nephritis in 8 (3.8%), other causes in 17 (7.9%) and unknown cause in 3 (1.9%) patients. During the 1990-2001 period, GN was recorded in only 101 (18%), PN in 90 (16.2%), DM in 138 (24.9%), nephrosclerosis in 82 (14.7%), polycystosis in 26 (4.7%), post-transplantation uremia in 28 (5.0%), lupus nephritis in 6 (1.1%), other causes in 65 (11.7%) and unknown cause in 20 (3.6%) patients. The mortality was caused by cardiac disease in 50.4%, cerebrovascular disease in 14.8%, infectious disease in 13.2%, malignancy in 7.5%, high potassium in 5.1%, gastrointestinal disease in 3.5%, other vascular diseases in 1.6%, cachexia in 1.3%, loss of blood access in 0.8%, other reasons in 1.1% and unknown reasons in 0.5% of patients. The results clearly indicate that the number of new patients grew and the mean patient age increased every year. Diabetes mellitus was the leading cause of uremia while GN and PN were less common. The main causes of death were cardiovascular diseases.

Adult↗

PubMed1990

Outcome of kidney transplantation in different diseases.

A. PATIENT SURVIVAL 1. The best cadaver graft patient survival 3-years posttransplant was observed in those whose primary disease was either nephrotic syndrome (98%), renal hypoplasia (98%), renal dysplasia (98%), IgA nephropathy (96%), or medullary cystic disease (97%). The worst survival was in those with Goodpasture's syndrome (88%), hypertensive nephrosclerosis (87%), MPGN (87%), IDDM (86%), and NIDDM (85%). 2. Patient survival correlated inversely with nonimmunologic graft loss. Nonimmunologic graft loss was high in patients with hypertensive nephrosclerosis (21%), polycystic kidney disease (23%), IDDM (27%), and NIDDM (27%). 3. Females with CGN and IDDM had better patient survival than males with the same diseases. The 2-, 3-, and 5-year survivals for females with IDDM were 91%, 89%, and 87% whereas for males, they were 87%, 84%, and 81%, respectively (p = 0.01). For CGN the 2-, 3-, and 5-year survivals were 95%, 94%, and 93% for females and 93%, 91%, and 90% for males (p less than 0.01). Females with Alport's syndrome had lower patient survival rates at 1 year (86%) than males (95%, p = 0.03). B. GRAFT SURVIVAL 1. The best 3-year graft survival was in recipients whose primary pathology was IgA nephropathy with 83% for cadaver grafts and 95% for LRD grafts. This was not secondary to center effects. The worst graft survival at 3 years for cadaver kidney recipients was in those whose primary illness was NIDDM (61%), hypertensive nephrosclerosis (58%), MPGN (59%), and Goodpasture's syndrome (59%).(ABSTRACT TRUNCATED AT 250 WORDS)

Cyclosporins↗

PubMedDate not supplied

An ultrastructural analysis of renal arterioles in benign and malignant essential hypertensions.

Renal arterioles from five patients with benign essential hypertension (BH) and four patients with malignant essential hypertension (MH) were studied using electron microscopy (EM). This study suggests a concept of different pathogenetic mechanism for renal vascular (arteriolar) lesions in BH and MH (i.e., benign and malignant nephrosclerosis, respectively) and does not support the idea of progression of benign nephrosclerosis to malignant nephrosclerosis. The EM technique has proven to be important in demonstrating specific changes characteristic of severe (or malignant) hypertension in the early stage in patients without clinical manifestation of MH, thus predicting a possibility of progressive histological change and clinical deterioration. This technique has clarified the light microscopy appearance of hyaline which continues to be an intriguing feature in the study of renal pathology.

Adolescent↗

PubMed1998

[Urinary excretion of glycosaminoglycans in patients with chronic pyelonephritis and chronic glomerulonephritis].

Glycosaminoglycanes (GAG) were measured in 24-h urine of patients with chronic pyelonephritis (CP) and chronic glomerulonephritis (CGN) at different stages of nephrosclerosis. These patients developed hyperglycosaminoglycanuria at early stages of nephrosclerosis before establishment of chronic renal failure. There is a positive correlation between the severity of excretion of GAG and leukocyturia in CP patients (p < 0.05). Estimation of GAG 24-h urinary excretion can help evaluate metabolism of connective tissue of the kidneys in CP and CGN patients for early diagnosis of nephrosclerosis, control of the treatment efficacy and the disease prognosis. It can also serve as additional criterion for rating of inflammation. The method is non-invasive, informative, available for clinical diagnostic laboratories.

Adult↗

PubMed1998

Clinical evidence of contralateral renal parenchymal injury in patients with unilateral atherosclerotic renal artery stenosis.

It has been postulated that the kidney contralateral to a significant renal artery stenosis may be at risk for accelerated arteriolar nephrosclerosis. Duplex ultrasound is capable of detecting and classifying renal artery stenosis and examining parenchymal flow. Renal flow patterns are a reflection of resistance, which increases with parenchymal pathology. One-hundred fifty-one patients with atherosclerotic renal artery stenosis (ARAS) were prospectively studied with duplex ultrasonography. Renal arteries were classified as normal, <60% stenosis, > or =60% stenosis, or occluded. The renal artery end-diastolic ratio (EDR) (end-diastolic velocity/peak systolic velocity) was measured. EDR decreases as resistance to flow increases. There were 81 patients with a unilateral > or =60% ARAS. The EDR was significantly lower in the kidney contralateral to the > or =60% ARAS (0.27 +/- 0.08 versus 0.30 +/- 0.08; p = 0.001, paired t-test). The absolute difference in EDR was even more pronounced in the subgroup of 15 diabetic patients with a > or =60% ARAS (0.22 +/- 0.08 versus 0.27 +/- 0.08; p = 0.004). This study offers clinical evidence that a unilateral hemodynamically significant ARAS is associated with the development of arteriolar nephrosclerosis in the contralateral kidney. These results have important implications on blood pressure control, renal function, and response to renal revascularization in this patient population.

Aged↗

PubMed2004

Hypertensive renal damage: insights from animal models and clinical relevance.

Investigations using chronic blood pressure (BP) radiotelemetry in conscious animals have provided substantial insights into the pathophysiology of hypertensive renal damage. Normal renal autoregulation protects the renal microvasculature from significant injury in most patients with primary hypertension, unless BP exceeds a certain threshold, when malignant nephrosclerosis develops. However, if autoregulation is impaired, as in chronic renal disease and/or diabetes models, the threshold for renal damage is lowered and glomerulosclerosis (GS) increases linearly with increasing BP. Modest BP reductions are predicted to prevent malignant nephrosclerosis, but prevention of GS in patients with diabetes and chronic renal disease requires that BP be lowered well into the normotensive range, as recognized in the currently recommended BP goals. When BP load is accurately assessed in these experimental models, renal protection is proportional to the achieved BP reductions, and there is little evidence of BP-independent protection, even with agents that block the renin-angiotensin system (RAS). Recent clinical data also suggest that achieving lower BP targets might be vastly more important than the choice of therapeutic regimens. Nevertheless, because aggressive diuretic use is usually necessary to achieve such BP goals, RAS blockade should be included as initial therapy both for antihypertensive synergy and to minimize the potassium and magnesium depletion associated with diuretics.

Animals↗

PubMed1979

Urinary prostaglandins in kidney disease.

Substances having the chromatographic behaviour and the bioassay properties of prostaglandins (PGE and PGF) were detected in the urine of 30 patients with kidney disease and 15 healthy subjects. The mean urinary PGE and PGF values in 15 patients with chronic glomerular disease or nephrosclerosis were significantly lower than those of 15 patients with chronic pyelonephritis and other forms of chronic interstitial nephritis, polycystic kidney disease, obstructive nephropathy or diuretic phase of acute renal failure, and of the mean PGE and PGF values found in the healthy subjects. It was suggested that in contrast to disease affecting primarily the renal medulla, chronic glomerular disease and nephrosclerosis are accompanied by a decrease of renal prostaglandin synthesis and/or release.

Glomerulonephritis↗

PubMed1992

Blood pressure related separately to parenchymal fibrosis and vasculopathy of the kidney.

The term nephrosclerosis is customarily used to designate a pathological entity that tends to characterize subjects with high blood pressure; it refers to a condition of diffuse fibrous replacement of renal substance secondary to ischemia from hypertension-related vascular injury. The features of parenchymal fibrosis can be distinguished from those of vasculopathies in tissue sections, parenchymal fibrosis being measured by assessing the degree of interstitial fibrosis and by counting obsolete glomeruli, while vasculopathies are measured by determining arterial intimal fibroplasia and by counting hyalinized arterioles. A series of 166 autopsies in subjects aged 25 to 92 years, selected because ample documentation of blood pressure was available, was assessed. One form of vasculopathy, arterial fibroplasia, is a better correlate of high blood pressure than is parenchymal fibrosis in this body of data. Cases with much vasculopathy and little parenchymal fibrosis occurred frequently, and these subjects were usually hypertensive. Cases with little vasculopathy and much parenchymal fibrosis were also encountered, but these subjects were usually not hypertensive. The suggested conclusion is that blood pressure relates less to the renoprival state of nephron loss than it does to renal ischemia in patients with nephrosclerosis.

Adult↗

PubMed1987

Proteinuria in hypertension.

It had been previously thought that protein excretion in hypertensive nephrosclerosis was less than 0.5 to 1.0 g/24 h. Furthermore, it was believed that proteinuria in the nephrotic range associated with hypertension was probably due to primary renal disease, malignant hypertension, renal artery stenosis, or pheochromocytoma. We report eight patients with biopsy-proven hypertensive nephropathy and heavy proteinuria in the absence of malignant hypertension or renal artery stenosis. The 24-hour protein excretion ranged from 2.7 to 4.3 g. All patients had renal insufficiency, with serum creatinine ranging from 2.0 (176.8) to 7.8 mg/dL (689.5 mumol/L). Renal function worsened in most patients during the follow-up period despite adequate control of the hypertension, and three patients had to be started on hemodialysis. Three patients died during the follow-up period. We conclude that hypertensive nephrosclerosis must be included in the differential diagnosis of marked proteinuria in patients with essential hypertension and that heavy proteinuria, along with renal insufficiency, are poor prognostic indicators in such patients.

Adult↗

PubMed1989

The pathogenesis of chronic renal failure.

The pathogenesis of terminal renal failure is discussed. The following are distinguished: 1. Renal failure occurring against a background of decompensated benign nephrosclerosis, primary and secondary malignant nephrosclerosis, and stenosis of the renal artery. 2. Renal failure caused by loss of glomeruli. It is pointed out that in most glomerulopathies, including diabetic glomerulopathy and renal amyloidosis, terminal renal failure only develops when accompanying disease of the postglomerular vessels leading to interstitial fibrosis impairs the outflow of blood from the glomerulus to such an extent that no more urine is produced. 3. Renal failure in disease of the tubules themselves. It is emphasized that acute renal failure only becomes chronic when interstitial fibrosis develops from the interstitial edema occurring in the early stage of the disease. 4. Renal failure occurring in primary diseases of the renal cortical interstitium. The chronic sclerosing renal diseases arising from acute interstitial nephritis are dealt with, as also are reflux nephropathy, incomplete obstructive nephropathy, analgesic nephropathy, and chronic interstitial rejection reactions in transplanted kidneys.

Diabetic Nephropathies↗

PubMed1999

Percutaneous renal biopsy: three years of experience with the biopty gun in 761 cases--a survey of results and complications.

From 1.1.1993 to 12.31.1995 we performed 761 consecutive biopsies on 509 non-selected patients. The most frequent diagnoses in 351 biopsies (39.4%) on native kidneys were 262 cases of glomerulonephritis (74.6%) and 167 of so-called benign nephrosclerosis (47.6%). With 410 biopsies (60.6%) on allograft kidneys 219 cases (78%) showed signs of interstitial rejection, 14 cases (5%) vascular and 49 cases (17%) interstitial as well as vascular rejection. Only after 5 biopsies (0.66%) clinical relevant complications (3 perirenal haematomas, 1 AV fistula, 1 vesical tamponade) appeared. Again percutaneous renal biopsy is proven to be a diagnostically efficient and safe tool at the same time even when used in a large number of non-selected patients, so that an ambulant performance may be discussed. The relatively frequent diagnosis of a so-called benign nephrosclerosis seems to indicate the need for an intensified examination of this disease.

Adult↗