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PubMedDate not supplied

[Status and development of the kidney after surgical treatment of hydronephrosis in children].

Development of the kidneys after correction of hydronephrosis was studied in 40 patients operated at the age of 8 months-12 years. Follow-up lasted 10-25 years. X-ray control showed efficiency of correction of the uretheropelvic segment (UPS). Roentgenoplanimetric study demonstrated a uniform 50-100% increase in renal area and its parenchyma in 28 patients (32 kidneys). In 9 patients parenchyma increased 2.5-4-fold, renal area by 50-100%. In three cases parenchyma diminished by 3-10% in growth of the kidney by 24-80%. This evidenced of nephrosclerosis progress. UPS correction favoured renal growth and development. There were only few cases when correction of UPS was positive but nephrosclerosis aggravated. Development of the kidney may depend on many factors such as preoperative condition of the kidney, severity of UPS obstruction, the patient's age, duration and severity of pyelonephritis, dysplasia and age-related immaturity of renal parenchyma, immune status of the organism, microorganism virulence, etc. But decisive was the condition of renal parenchyma before the operation. In 3 patients with progressive nephrosclerosis renal parenchyma affection was additionally characterized by advanced sclerosis and inflammatory infiltration of the intertitium which ended in a poor outcome. The above observations suggest the necessity of long-term postoperative follow-up of the patients to design effective measures aimed at the treatment and prevention of nephrosclerosis.

Adolescent↗

PubMed1977

[Immunohistological findings in non-glomerulonephritic renal disease (author's transl)].

Immunohistological study of 123 kidney biopsies of non-glomerulonephritic kidney diseases showed that deposits of immunoglobulins are found more often in cases of malignant than in cases of benign nephrosclerosis. Primary malignant nephrosclerosis is mostly associated with glomerular deposits of immunoglobulins. Positive immunohistological findings are frequent in cases of diabetic glomerulosclerosis, mainly within glomeruli, but also in tubular basement membranes and Bowman's capsule. In cases of glomerular amyloidosis we see cloudy-bandlike deposits, but are unable to differentiate cases with or without the nephrotic syndrome. If we consider an immunopathogenetic mechanism for the diseases discussed in terms of the present findings, it seems possible for primary malignant nephrosclerosis as well as for certain glomerular changes associated with acute renal failure or rejection of transplants. In diabetic glomerulosclerosis (apart from special forms with perimembranous lesions) and glomerular amyloidosis, we consider such a mechanism to be unlikely. By separating the non-glomerulonephritic diseases into different types of deposits we found pictures that correspond with immunocomplex diseases. Pictures resembling anti-basement membrane diseases have not been seen. Characteristic patterns of deposits were not found, thus immunohistology is without additional diagnostic value in the field of non-glomerulonephritis disease.

Acute Kidney Injury↗

PubMed1982

Fetal outcome in hypertensive disorders of pregnancy.

Fetal outcome was evaluated in 157 hypertensive pregnant women whose underlying disease had been established by renal biopsy. The patients had pathologic diagnoses of preeclampsia (95), nephrosclerosis (23), nephrosclerosis with superimposed preeclampsia (13), interstitial and tubular nephropathy (seven), and normal findings (six). Pregnancy outcome in this selected group of patients was extremely poor, with the perinatal mortality rate being 134 per 1,000. There were 21 perinatal deaths; three quarters of these were stillbirths, and most were encountered below the fiftieth weight percentile and before 30 weeks' gestation. In addition 22% of the infants were small for gestational ages, and 40% of the infants were born before term. Most of the perinatal mortality (81%) was in women with preeclampsia. The worst fetal outcome was encountered in multiparous preeclamptic women, over 50% of whom manifested nephrotic-range proteinuria during pregnancy. Despite the presence of hypertension throughout most of their gestation, women with nephrosclerosis alone had the best fetal survival rate.

Apgar Score↗

PubMed2003

Hypertensive risk factors in kidney disease in African Americans.

African Americans with hypertension more commonly develop renal insufficiency compared to Caucasians. The African American Study of Kidney Disease (AASK) included a renal biopsy pilot study that demonstrated that the clinical diagnosis of so-called hypertensive nephrosclerosis in these African American patients indeed was accurate. This biopsy study demonstrated extensive global glomerulosclerosis, far exceeding that expected for patients' age. We further compared our clinically indicated renal biopsies to determine if any phenotypic differences were present in hypertensive nephrosclerosis in African Americans versus Caucasians. These studies point to an excess of the solidified type of global glomerulosclerosis (GS) (also called "decompensated benign nephrosclerosis") in African Americans compared to more obsolescent type GS in Caucasians. We speculate that these phenotypic differences might reflect differing mechanisms of tissue injury in hypertensive African Americans versus Caucasians, and discuss possible contributors to this injury.

Black or African American↗

PubMed2004

Trends in incidence of end-stage renal disease in Japan, 1983-2000: age-adjusted and age-specific rates by gender and cause.

BACKGROUND: Trends in age-adjusted or age-specific incidence rates of end-stage renal disease (ESRD) have never been examined in Japan, a major ESRD epidemic area. METHODS: A nationwide registry has provided the number of ESRD patients commencing maintenance renal replacement therapy for time period from 1983 to 2000. We computed gender- and age-specific incidence rates of ESRD over 2-year periods, in total or by cause. Age-adjusted incidence rates were calculated using the 1985 Model Population of Japan as the standard. RESULTS: Causes of ESRD in 1999-2000 were, in order of decreasing frequency, diabetic nephropathy, chronic glomerulonephritis, unknown causes, nephrosclerosis and polycystic kidney disease in men, and chronic glomerulonephritis, diabetic nephropathy, unknown causes, nephrosclerosis and polycystic kidney disease in women. The age-adjusted all-cause incidence of ESRD increased until 1995-1996, but has since levelled off in both genders. The age-adjusted rate for diabetic nephropathy has been rapidly increasing, while that for chronic glomerulonephritis has decreased since 1995-1996. The former rate exceeded the latter in 1997-1998 in men. All-cause ESRD has rapidly increased in the eighties age group, whereas the increase slowed down in younger age groups in the late 1990s. The rate for diabetic nephropathy has linearly risen in almost every age group in men, whereas it began to level off in women aged 40-59 years at about 1995. For chronic glomerulonephritis, the rate had already started to decline in the mid-1980s in those aged <45 years. The rate of nephrosclerosis has been increasing independently of age. CONCLUSIONS: The present study shows changes in the epidemiological features of the incidence of ESRD in Japan from 1983 to 2000.

Adult↗

PubMed2002

Sustained expression of thrombospondin-1 is associated with the development of glomerular and tubulointerstitial fibrosis in the remnant kidney model.

BACKGROUND/AIMS: Transforming growth factor-beta1 (TGF-beta1) has been implicated in the development of progressive nephrosclerosis in the remnant kidney model of chronic renal insufficiency. Thrombospondin-1 (TSP-1) is an extracellular matrix protein which has been recently shown to be capable of converting TGF-beta from its latent to its active form. We studied the expression of TSP-1 mRNA and protein during the development of glomerular and tubulointerstitial nephrosclerosis in the renal ablation model particularly in relation to TGF-beta1 expression. METHODS: The remnant kidney model in the rat was investigated 3 days, 1 week, 2 weeks, 3 weeks, 4 weeks, 7.5 weeks and 10 weeks after disease induction. Using single and double immunostaining techniques, renal tissues were examined for TSP-1 protein, TGF-beta1, platelet-derived growth factor BB, extracellular matrix proteins, such as collagens and fibronectin, myofibroblast formation and macrophage influx. TSP-1 mRNA expression was investigated using a radioactive in situ hybridization technique. RESULTS: De novo expression of TSP-1 mRNA and protein occurred in all glomerular cell types as well as in tubular cells, myofibroblasts and some macrophages in areas of tubulointerstitial injury. TSP-1 expression preceded and was sustained during the development of tubulointerstitial and glomerular fibrosis and was frequently localized at sites of increased expression of TGF-beta1, but not of platelet-derived growth factor BB. CONCLUSION: In the remnant kidney model, the time course and localization of TSP-1 are consistent with its playing a role as a local activator of TGF-beta1, thereby potentially participating in the development of nephrosclerosis.

Animals↗

PubMed2002

Nephrotic proteinuria as a result of essential hypertension.

BACKGROUND: The presence of nephrotic-range proteinuria in a nondiabetic hypertensive patient is generally indicative of an underlying glomerular disease. A few published reports have noted nephrotic proteinuria in some patients with hypertensive nephrosclerosis. The frequency of this association is unknown. METHODS: We retrospectively reviewed renal biopsy reports on all cases of nephrotic syndrome over an 8-year period (1993-2000). We excluded all cases of diabetes mellitus, lupus, hepatitis, human immunodeficiency virus, and chronic use of nonsteroidal anti-inflammatory drugs. Biopsy specimens showing glomerular eosinophilic hyalinosis lesions, positive immunofluorescence staining, or dense deposits on electron microscopy were also excluded. Thirteen of the remaining 237 (5.5%) biopsy specimens satisfied the standard histological criteria for hypertensive nephrosclerosis. RESULTS: All patients were African-Americans with a mean age of 47.5 +/- 13 years and an average mean arterial blood pressure of 122 +/- 19 mm Hg. The mean values for urinary protein excretion, serum creatinine, albumin, and cholesterol were 8.9 g/day, 3.3 mg/dl, 3.1 g/dl, and 245 mg/dl, respectively. Optimal blood pressure control required at least three antihypertensive agents. Progression to end-stage renal disease occurred over a mean duration of 8.3 +/- 6.5 months. Multivariate regression showed a strong but nonsignificant association between the level of proteinuria at the time of biopsy, duration of hypertension, and number of blood pressure medications (R(2) = 0.56, p = 0.38). CONCLUSIONS: Nephrotic syndrome may be more common in poorly controlled essential hypertension than previously realized. In African-American patients, the differential diagnosis of nephrotic syndrome should include hypertensive nephrosclerosis, but abrogation of renal biopsy is not implied.

Adult↗

PubMed2005

Differential effects of antihypertensive drugs on renal and glomerular hemodynamics and injury in the chronic nitric-oxide-suppressed rat.

BACKGROUND/AIMS: Prolonged nitric oxide synthase (NOS) inhibition with N(omega)-nitro-L-arginine methylester in normotensive and hypertensive rats has been demonstrated to produce severe systemic and glomerular hypertension with glomerular sclerosis, and these changes have become a useful experimental model of hypertensive nephrosclerosis. This review summarizes data from our serial studies as well as work of others who are also investigating the effects of the commonly used antihypertensive drugs (including calcium antagonist, angiotensin-converting enzyme inhibitor, angiotensin II type 1 receptor blocker, aldosterone antagonist and thiazide diuretic) on renal and glomerular hemodynamics, renal function and glomerular histopathology using this model. METHODS: A Medline search was performed to identify the relevant literature describing renal effects of antihypertensive drugs in models of hypertension and nephrosclerosis produced or exacerbated by NOS inhibition. RESULTS: Existing data have indicated that most of these drug classes have produced dramatic renoprotective effects, structurally or functionally, on nephrosclerosis induced by prolonged NOS inhibition. CONCLUSION: This review of experimental studies has provided strong evidence supporting the clinical benefits of antihypertensive drugs for hypertensive patients with renal impairment particularly those with endothelial dysfunction associated with NOS deficiency.

Animals↗

PubMed2002

Activation of the Fas/Fas ligand pathway in hypertensive renal disease in Dahl/Rapp rats.

BACKGROUND: Hypertensive nephrosclerosis is the second most common cause of end-stage renal failure in the United States. The mechanism by which hypertension produces renal failure is incompletely understood. Recent evidence demonstrated that an unscheduled and inappropriate increase in apoptosis occurred in the Dahl/Rapp rat, an inbred strain of rat that uniformly develops hypertension and hypertensive nephrosclerosis; early correction of the hypertension prevents the renal injury. The present study examined the role of the Fas/FasL pathway in this process. METHODS: Young male Dahl/Rapp salt-sensitive (S) and Sprague-Dawley rats were fed diets that contained 0.3% or 8.0% NaCl diets. Kidneys were examined at days 7 and 21 of the study. RESULTS: An increase in Fas and FasL expression was observed in glomerular and tubular compartments of kidneys of hypertensive S rats, whereas dietary salt did not change expression of either of these molecules in normotensive Sprague-Dawley rats. Associated with this increase was cleavage of Bid and activation of caspase-8, the initiator caspase in this apoptotic pathway, by day 21 of the study. CONCLUSIONS: Augmented expression of apoptotic signaling by the Fas/FasL pathway occurred during development of end-stage renal failure in this model of hypertensive nephrosclerosis.

Animals↗

PubMed1983

Hemolytic-uremic syndrome in an adult.

This report describes a 45-year-old man who suffered from hemolytic-uremic syndrome. In his autopsy findings, kidney arteriolar walls showed marked hyaline degeneration and interlobular arteries were occluded by severe intimal proliferation. No vascular changes were found in other organs. There were no arteriosclerotic changes in either main branches from the aorta or the aorta. These vascular changes are correspond well with the early features of malignant nephrosclerosis without any clinical findings of malignant hypertension. This type is called primary malignant nephrosclerosis by Bohle et al. We would like to point out the significance of this case in the re-consideration of the pathogenesis of malignant nephrosclerosis.

Hemolytic-Uremic Syndrome↗

PubMed1992

Renal consequences of arterial hypertension.

AIM: To seek ways of improving the prognosis for renal function in the presence of arterial hypertension. BACKGROUND: Nephrosclerosis is a term used to define the renal damage induced by arterial hypertension. The renal vasculature can participate in the genesis of essential hypertension and can suffer the consequences of elevated blood pressure. There is no doubt that antihypertensive therapy has dramatically improved the prognosis for renal function in the presence of arterial hypertension. RESULTS OF LITERATURE REVIEW: There appears to be a need for a further improvement in the prognosis for renal hypertension. At present, the prevalence of nephrosclerosis as a cause of terminal renal failure may be increasing and a progressive fall in renal function in treated hypertensive patients compared to normotensives has been described. CONCLUSIONS: It is not yet clear whether improvements in renal hypertension depend merely on the effectiveness of antihypertensive therapy in reducing arterial blood pressure or whether it will be necessary to improve the metabolic disturbances that accompany hypertension or the renal hemodynamic effects of different drugs before the prognosis for nephrosclerosis can be improved.

Antihypertensive Agents↗

PubMed1991

The renal histopathology of essential malignant hypertension in black South Africans.

The renal histopathology of essential malignant phase hypertension in two groups of black South Africans was studied. The first, an autopsy series, consisted of material obtained in 1956-1961, a period when adequate antihypertensive therapy had not yet become generally available. The second group, a renal biopsy series, was from an era when effective antihypertensive therapy was available (1979-1989). The study showed that the clinical and histopathological changes of malignant hypertension were similar in both the pre-treatment and treatment eras. Fibrinoid necrosis was found in 92% of the autopsy sections and 44% of the biopsies. While mucinous, onion-skin and fibrotic changes of the blood vessels were commonly found, they were not invariably present and could not be considered the histopathological hallmark of malignant nephrosclerosis. It was often impossible on histological examination to distinguish malignant nephrosclerosis arising de novo from that superimposed on long-standing previous benign hypertension. Replication of internal elastic lamina, which has been considered a marker of long-standing previous benign hypertension, was a nonspecific finding and was frequently observed in young hypertensive subjects with a short clinical history. When fibrinoid necrosis is present, diagnosis of malignant nephrosclerosis can be made with confidence in black South Africans.

Adult↗

PubMed1997

[Hydrocortisol, parathyroid hormone and calcitonin in blood of patients with chronic pyelonephritis and nephrosclesosis].

Hydrocortisole, parathyroid hormone (PTH), and calcitonin were radioimmunoassayed in the blood of patients with chronic pyelonephritis. Hydrocortisone content decreased at the early stages of nephrosclerosis before renal failure, and hypercalcitoninemia was developing. In chronic renal insufficiency hydrocortisone level normalized, hypercalcitoninemia augmented, and PTH level in the blood plasma increased. Disorders of these substances metabolism are believed to be one factor in the pathogenesis of pyelonephritic nephrosclerosis. Measurements of blood hydrocortisone and calcitonin in patients with chronic pyelonephritis can be used for early diagnosis of nephrosclerosis before its clinical manifestation as chronic pyelonephritis. Such measurements will help objectively assess the activity of the sclerotic process, timely begin proper treatment, and predict the disease course and outcome.

Adult↗

PubMed2000

Chronic proteinuric nephropathies: outcomes and response to treatment in a prospective cohort of 352 patients with different patterns of renal injury.

The Ramipril Efficacy in Nephropathy (REIN) study found that angiotensin-converting enzyme (ACE) inhibitors effectively decreased proteinuria, glomerular filtration rate (GFR) decline (DeltaGFR), and incidence of end-stage renal disease (ESRD) in patients with proteinuric chronic nephropathies. In this study, we prospectively investigated the main clinical determinants of progression and response to treatment in the 352 patients enrolled into the REIN study. Mean DeltaGFR (0.56 +/- 0.05 [SEM] versus 0.21 +/- 0.05 mL/min/1.73 m(2)/mo; P = 0.0001) and incidence of ESRD (30% and 10%; P = 0.0001) were more than twice that in patients with proteinuria of 2 g/24 h or greater of protein compared with those with protein less than 2 g/24 h (relative risk [RR], 4.07; 95% confidence interval [CI], 2.20 to 7.52), as well as in patients with hypertension compared with normotension (mean DeltaGFR, 0.48 +/- 0. 05 versus 0.22 +/- 0.05 mL/min/1.73 m(2)/mon; P = 0.0006; ESRD, 25% versus 10%; P = 0.004; RR, 3.18; 95% CI, 1.38 to 7.32). Hypertension at study entry (P = 0.038), greater mean blood pressure on follow-up (P = 0.002), and urinary protein excretion rate (P = 0.0001) were independent predictors of faster DeltaGFR. DeltaGFR was approximately twofold faster in patients with type 2 diabetes than in those with primary glomerular disease (P = 0.002; including immunoglobulin A [IgA] nephropathy, P = 0.009); nephrosclerosis (P = 0.03), adult polycystic kidney disease (APKD), or chronic interstitial nephritis (P = 0.006). Diabetes at study entry (P = 0. 02) and greater mean blood pressure (P = 0.0001) and urinary protein excretion rate (P = 0.0001) on follow-up were independent predictors of faster DeltaGFR. After correction for baseline covariates, diabetes was also associated with an increased risk for progression to ESRD (RR, 2.39; 95% CI, 1.01 to 5.68; P < 0.05). At multivariate analyses, ramipril significantly decreased DeltaGFR (regression coefficient,-0.23 +/- 0.11 [SEM]; P = 0.036) and ESRD (RR, 2.08; 95% CI, 1.21 to 3.57; P = 0.008) in patients with baseline proteinuria of 2 g/24 h or greater of protein, and the renoprotective effect increased for increasing levels of proteinuria. Ramipril decreased DeltaGFR to a similar extent in normotensive and hypertensive patients (-0.14 +/- 0.11 versus -0.14 +/- 0.09) and significantly limited ESRD in hypertensive patients (RR, 2.03; 95% CI, 1.26 to 3. 26; P = 0.004). DeltaGFR was decreased by 42% in primary glomerular disease (P = 0.017), by 35% in IgA nephropathy, and by 37% in nephrosclerosis, but was not improved in type 2 diabetes, APKD, or interstitial nephritis. At multivariate analyses, ramipril significantly slowed DeltaGFR (-0.24 +/-0.08; P = 0.004) and progression to ESRD (RR, 2.32; 95% CI, 1.36 to 3.96; P = 0.002) in patients without diabetes, but not in patients with diabetes, who tended to have a faster DeltaGFR (+0.62 +/- 0.44) on ramipril therapy. In summary, patients with proteinuria of 2 g/24 h or greater of protein, preexisting hypertension, or type 2 diabetes were faster progressors. Greater blood pressure and degree of proteinuria were the strongest determinants of faster GFR decline. The renoprotective effect of ramipril was similar in patients with normotension and hypertension. Hypertensive patients and those with proteinuria of 2 g/24 h or greater of protein, primary glomerular disease, or nephrosclerosis gained the most from ACE inhibitor treatment. During the study period, those with proteinuria less than 2 g/24 h of protein, type 2 diabetes, or polycystic kidney disease did not benefit by treatment to an appreciable extent.

Adolescent↗

PubMed1994

Race, socioeconomic status, and the development of end-stage renal disease.

The reasons for the increased annual incidence of end-stage renal disease (ESRD) in blacks compared with whites are unclear, but may include lack of access to treatment of the causative disease, which likely relates closely to socioeconomic status (SES). End-stage renal disease rates for diabetic glomerulosclerosis, hypertensive nephrosclerosis, and glomerulonephritis were determined in the 9,390 black and white New York State residents who began treatment within the Medicare program between 1982 and 1988. The relationship between the incidence of ESRD, age, and SES, as measured by the race-specific median family income in the patient's zip code, was estimated using a series of logistic-regression models for 12 populations: three causes of renal failure by two races by two sexes. For whites, incidence rates of diabetic glomerulosclerosis and hypertensive nephrosclerosis were significantly negatively associated with declining SES for the 45 to 65 year and 25 to 55 year age groups, respectively. In contrast, there was no relationship between the incidence of these diseases and SES in blacks. For glomerulonephritis, effects of SES were minor for both races. Better access to treatment of diabetes and hypertension might well decrease the annual incidence of ESRD due to diabetic glomerulosclerosis and hypertensive nephrosclerosis in whites. If the SES measures used for blacks are adequate, predisposition to progressive renal damage in response to renal injury or environmental factors other than SES are stronger risk factors for ESRD than SES.

Adult↗

PubMed2002

Influence of arteriolar hyalinization on arterial intimal fibroplasia in the renal cortex of subjects in the United States, Peru, and Bolivia, applicable also to other populations.

Microvasculopathies of nephrosclerosis progress with age in contrasting patterns. Arterial intimal fibroplasia (R(r) and R(c), respectively, in small and large interlobular arteries) previously showed close linkages to hypertension and to "nephrosclerosis," defined by fibrous replacement of atrophied nephrons, whereas hyalinization of arterioles (Hy) failed to show consistent linkages. In this study, renal samples from seven populations, three newly assembled and four reassessed from archived data, were evaluated for R(r), R(c), and Hy in forensic autopsies of basal subjects (ie, those lacking conditions known to correlate with hypertension or nephrosclerosis, mostly deaths by violence). The patterns of progression on age were alike in all populations, but the rates of progression differed greatly. The observed ranges indicate a 547% higher rate for Hy in the fastest compared with the slowest population, a 49% higher rate for R(c), and a 107% higher rate for R(r). About one third of variation in R(r) and R(c) between populations can be attributed to the correlation with Hy, leaving a substantial residual effect independent of Hy. The findings suggest that the etiology propelling hyalinization in arterioles seems somehow to accelerate the progression of intimal fibroplasia in arteries. The reverse direction, fibroplasia somehow accelerating hyalinization, seems unreasonable, because the presumed consequence, Hy, fails to increase notably with age after 40 years, whereas the presumed causes, R(r) and R(c), rise unremittingly into old age. The etiologies of the population differences are of great consequence to public health but remain unknown.

Adolescent↗

PubMed2002

Significance of age in the survival of diabetic patients after kidney transplantation.

BACKGROUND: In recent years acceptance of diabetic patients for renal replacement therapy has increased. Renal transplantation for Type I diabetic patients is widely accepted but the appropriate treatment for Type II diabetic patients is still a matter of dispute. Our study was done to determine whether the age of Type II diabetic patients constituted an additional risk factor. METHODS: We analyzed the outcome of renal transplantation in 56 diabetic patients, 31 Type I and 25 Type II diabetics (we excluded any who had combined kidney-pancreas transplants). We compared them with 51 non-diabetic patients who were transplanted because of end-stage renal failure due to nephrosclerosis and age-matched to type II diabetic patients. We assessed the one- and three-year patient and graft survival, the quality of renal function, the main complications and causes of mortality. RESULTS: The overall one- and three-year patient survival was 69% and 60% in Type II patients; 73% and 69% in Type I diabetes patients and 88% and 80% in patients with nephrosclerosis. The overall one- and three-year actuarial graft survival was 50% and 38% in patients with Type II disease and 58% and 50% in Type I diabetes, and 76% and 64% in nephrosclerosis. The main cause of graft loss in all groups was death (with functioning kidney) due to infections and cardiovascular complications. CONCLUSIONS: Diabetes itself is the most important variable in patients who have poor results after kidney transplantation. Increasing age increases slightly the risk for poor graft and patient survival. Both groups of diabetic patients have poorer results than controls but in this comparison age was an independent factor.

Adult↗

PubMed2001

Franz Volhard and Theodor Fahr: achievements and controversies in their research in renal disease and hypertension.

The clinician, Franz Volhard, and the pathologist, Theodor Fahr, worked closely together in Mannheim from 1909 until 1915 and introduced a novel classification of renal diseases. In the monograph entitled 'Die Bright'sche Nierenkrankheit, Klinik, Pathologie und Atlas' (1914) they differentiated between degenerative (nephroses), inflammatory (nephritides) and arteriosclerotic (scleroses) diseases. Nephrosclerosis was divided into the benign and malignant form, of which the latter stood the test of time as a new disease entity. Fahr further divided benign nephrosclerosis into the compensated and decompensated form--depending on the presence or absence of glomerular injury. In the pathogenesis of malignant nephrosclerosis, Volhard stressed the decisive role of severe blood pressure elevation, while Fahr postulated an inflammatory mechanism, a concept later confirmed by Adalbert Bohle for at least a minority of patients. A very far reaching concept of Franz Volhard was his idea that pale (renal) hypertension results from a pressor substance released from ischaemic kidney(s) contributing--via a vicious circle--to a further rise in blood pressure with subsequent renovascular injury and aggravation of hypertension. This hypothesis was supported in 1930 by initial experiments of his collaborator, Hartwich (demonstrating in dogs a mild rise in blood pressure after ligation of branches of the renal artery) and definitively proven by Goldblatt (1934) in dogs by induction of severe and persistent hypertension after clamping of both renal arteries. The consequent detection of the renin angiotensin system was the final confirmation of Volhard's postulated renal pressor substance. In the pathogenesis of red (essential) hypertension, Volhard stressed the role of hereditary factors, age, obesity and potentially of severe alcoholism. He emphasised a premature reduction of vascular distensibility (due to elastosis of the prearterioles), a high cardiac output as well as a dampening of baroceptor function. Additionally, Volhard made crucial advances in cardiology and pneumology. Journal of Human Hypertension (2001) 15, 5-16

Germany↗