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PubMed1994

Recognition and management of reversible renal failure.

This review will address five selected conditions associated with variable degrees of renal insufficiency or renal failure. Early diagnosis, usually possible in the office setting, should encourage early treatment and/or referral that will be rewarded by substantial improvement or return of normal renal function. Hypertensive nephrosclerosis, particularly among black Americans, is now the second leading cause of end stage disease (ESRD) in the United States. Aggressive treatment of hypertension can prevent progression to renal failure. Obstructive uropathy is relatively common at all ages; if not corrected, it can progress insidiously, often without symptoms, to destruction of a kidney. Glomerulonephritis may involve the kidneys primarily or in association with a multisystem disorder. Early renal biopsy will help establish the pathologic diagnosis and guide subsequent therapy. The kidney is vulnerable to the nephrotoxic effects of numerous pharmacologic agents used commonly in the diagnosis and treatment of illness. Potential nephrotoxicity to a given class of agents must be recognized if progressive nephrotoxicity is to be avoided. Finally, the frequency of occlusive renovascular disease and ischemic nephropathy is on the rise as the US population increases in age. Several interventions are available for the treatment of ischemic nephropathy and for the prevention of ESRD associated with bilateral renal artery occlusion.

Arteriosclerosis↗

PubMed1987

Possible causes and consequences of hypertension in stable renal transplant patients.

Previous epidemiologic studies of hypertension in renal transplant patients have produced contradictory results. Therefore, the incidence and clinical setting of chronic hypertension were examined in 201 stable renal transplant patients using a multivariate approach. Hypertension was present in 52.7% of patients at one year, and in 46.3% at the time of last follow-up, 5.0 +/- 1.9 years (mean +/- SD) after transplantation. Among possible causative factors, discriminant analysis demonstrated that body weight, the presence of native kidneys, and variables linked to allograft function were most closely associated with hypertension at both one year and last follow-up. One year after transplantation, age, sex, pretransplant hypertensive nephrosclerosis, and diabetes were also independently associated with hypertension. However, renal function declined to a greater degree in hypertensive patients, and only body weight, the presence of native kidneys, and variables linked to allograft function were associated with hypertension at last follow-up. Results also demonstrated that hypertension was associated with elevated serum lipid levels and an increased likelihood of dying or returning to dialysis. Thus, these results suggested several important risk factors for hypertension and its consequences in renal transplant patients.

Adult↗

PubMed1990

Impact of race on renal transplant outcome.

The influence of race on the outcome of cadaver renal transplantation (CRT) continues to be controversial even in the cyclosporine era. The present study examines the effect of race in 343 adult CRT performed from 1/1/82 through 10/1/88 with regard to the incidence of delayed function (DF), graft survival (GS), and patient survival (PS). Blacks constituted 38% of the patients. A history of nephrosclerosis secondary to hypertension was more common in blacks, with 51% (67/130) vs. 8% (17/213) in whites, while glomerulonephritis and Type 1 diabetes mellitus were more common in whites. There was no significant difference in the number of HLA (A,B,DR) matches or DR mismatches between whites and blacks. With azathioprine immunosuppression DF was more common in blacks than in whites, 54% (14/26) vs. 20% (11/55) respectively (P less than 0.01). The higher incidence of DF in blacks than in whites on Aza was associated with a significantly lower dose of intraoperative albumin, 0.25 g/kg vs. 0.44 g/kg, respectively (P less than 0.01). Of the Aza treated black recipients who had DF, 79% (11/14) had graft loss within three months, significantly worse than 25% (3/12) with graft loss when immediate function was present (P less than 0.005). Currently, all patients receive at least 0.80 g/kg of albumin intraoperatively and CsA quadruple induction therapy. With the current regimen, black and white recipients of primary CRT recipients have a comparable low incidence of DF of 18% and 22%, respectively. However, DF remains high among repeat black or white recipients: 33% (10/30) and 57% (8/14), respectively. The incidence of rejection within 30 days was similar for black and white recipients during the Aza and CsA eras, 62% vs. 75% and 34% vs. 42% respectively. GS and PS at three months for blacks on Aza were 54% and 89%, respectively, reflecting the corresponding high incidence of DF. This compares with 71% and 97% GS and PS for whites on Aza. Blacks and whites receiving CsA had equivalent 1-year GS and PS: 76% and 92%, respectively. We conclude that, in our center during the Aza era, blacks had a higher incidence of DF and lower GS than whites. With our current intraoperative fluid replacement and CsA immunosuppression, the incidence of DF and GS and PS are equivalent in black and white recipients.

Azathioprine↗

PubMed1995

Glomerulosclerosis as a determinant of posttransplant function of older donor renal allografts.

Transplantation of kidneys from older donors is being advocated to expand the organ donor pool. However, the prevalence of atherosclerosis and age-induced renal structural alterations account for the variable function of allografts procured from these older donors. Pretransplant biopsies are sometimes used to evaluate kidneys from older donors, but to date there are no defined criteria correlating the extent of structural alterations in these kidneys to subsequent function. We investigated the effect of glomerulosclerosis, a marker for nephrosclerosis, on graft outcome. Sixty-five baseline biopsies of kidney allografts were retrospectively analyzed to identify a referent point of glomerulosclerosis that correlated with inferior graft outcome. Age and death from nontraumatic cerebrovascular injuries were the main correlates for donor glomerulosclerosis (P < 0.001). Allografts with poor function at 6 months defined as serum creatinine > 2.5 mg/dl (n = 13) or nephrectomy (n = 4) had a mean of 20% glomerulosclerosis at the time of implantation compared with only 2% sclerosis in allografts with good function (P < 0.05). Delayed graft function occurred in 22% and 33% of recipients with no glomerulosclerosis and those with less than 20% glomerulosclerosis, respectively. In contrast, patients receiving kidneys with > 20% sclerosis had an 87% incidence of delayed function (P < 0.05). Moreover, graft loss occurred in 7% of recipients of kidneys with less than 20% sclerosis and in 38% of recipients with > 20% sclerosis (P < 0.04). Measurements of serum creatinine in the donors did not distinguish the different degrees of glomerulosclerosis found on biopsy. Our data indicate that donor glomerulosclerosis greater than 20% increases the risk of delayed graft function and poor outcome of transplanted kidneys. Therefore, we advocate the use of routine biopsies of kidneys from older (> 50 yrs) donors and those donors with nontraumatic cerebrovascular accidents, despite seemingly normal preprocurement serum creatinine.

Adolescent↗

PubMed1995

Chronic renal allograft rejection in the first 6 months posttransplant.

Between May 1, 1986 and May 31, 1992 at the University of Minnesota, we interpreted 129 renal allograft biopsy specimens (done in 48 grafts during the first 6 months posttransplant) as showing changes consistent with chronic rejection. For this retrospective analysis, we reexamined these biopsies together with clinical information to determine: (a) whether a diagnosis other than chronic rejection would have been more appropriate, (b) how early posttransplant any chronic rejection changes occurred, and (c) if the diagnosis correlated with outcome. We found that (1) chronic rejection is uncommon in the first 6 months posttransplant; it was documented in only 27 (2.4%) of 1117 renal allografts and was preceded by acute rejection in all but 3 recipients (for these 3, the first biopsy specimen showed both acute and chronic rejection). (2) Chronic vascular rejection was seen in 1 recipient as early as 1 month posttransplant; the incidence increased over time and was associated with an actual graft survival rate of only 35%. (3) The most frequent cause of arterial intimal fibrosis in the first 6 months posttransplant was arteriosclerotic nephrosclerosis (ASNS) of donor origin. Long-term graft function for recipients with ASNS was 67%. (4) Early-onset ischemia or thrombosis was seen in 14 recipients and predicted poor outcome: only 35.7% of these recipients had long-term graft function. (5) Cyclosporine (CsA) toxicity was implicated in only 3 recipients, who had mild diffuse interstitial fibrosis in association with elevated CsA levels. Other variables (including systemic hypertension, urinary tract infection, obstructive uropathy, neurogenic bladder, cobalt therapy, and recurrent disease) were not significantly associated with chronic renal lesions in the first 6 months posttransplant. A significant number of biopsies were originally interpreted as showing chronic rejection, but the diagnosis was changed upon reevaluation in conjunction with clinical data. We conclude that many factors coexist to produce chronic lesions in biopsies during the first 6 months posttransplant, so clinical correlation is needed before establishing a diagnosis of chronic rejection.

Adolescent↗

PubMed1995

Renal toxicity of albumin and other lipoproteins.

Proteinuria may be an independent risk factor for nephrosclerosis. One potential mechanism has emerged with the finding that lipoproteins, including albumin, modulate the biology of mesangial cells and proximal tubular epithelial cells when internalized. Consequent alterations in renal-cell lipid metabolism may underlie some of these effects.

Albumins↗

PubMed1996

Hypertension and renal dysfunction.

The various end-stage renal disease registries have documented a progressive and substantial increase of hypertension as a cause of renal failure. However, the relationship between essential hypertension and progressive renal disease is unclear. Black hypertensive patients, who are more prone to renal failure during their middle age, have a peculiar hypertensive nephropathy possibly requiring an aggressive antihypertensive therapy. Hypertension-associated progressive renal disease in the Caucasian population usually appears in the elderly and may be related to atheromatous renovascular disease. Only a few hypertensive patients have a true progressive hypertensive nephrosclerosis.

Disease Progression↗

PubMed2003

Kidney disease, genotype and the pathogenesis of vasculopathy.

PURPOSE OF REVIEW: The two leading causes of end-stage renal disease in the United States are diabetes mellitus and hypertensive nephrosclerosis, accounting for over two-thirds of all cases. In many patients both diseases are associated with small- and large-vessel disease, commonly attributed to hypertension or accelerated atherosclerosis. Recent investigations, however, have suggested that renal large-vessel and microvascular disease may be independent contributors to progressive kidney failure. RECENT FINDINGS: Although genes have not been definitely linked to renal vascular disease, population- and family-based epidemiology of kidney disease, segregation analysis of Pima and Caucasian families in which diabetic nephropathy is clustered, and the positional cloning of genes responsible for rare, familial glomerulosclerosis syndromes support the hypothesis that genes regulate the pathogenesis of renal disease. This review highlights developments in our current understanding of vasculopathy and its role in renal disease, and it summarizes evidence suggesting that genetic determinants for the vascular phenotype are associated with common causes of chronic renal failure. SUMMARY: With the application of genomics and proteomics methodologies to drug discovery, the identification of renal susceptibility genes should identify new mechanisms of progressive renal disease pathogenesis and generate novel target molecules for the treatment of kidney disease.

Animals↗

PubMed2004

Renal endothelial effects of antihypertensive therapy.

PURPOSE OF REVIEW: To review the influence of antihypertensive therapy on the contribution of nitric oxide (NO) to renal perfusion in essential hypertension. RECENT FINDINGS: The contribution of endothelium-derived NO to renal perfusion can be examined in detail by studying isolated glomerular arterioles and by immunohistochemical techniques. Only few functional studies in human arterial hypertension exist analysing the role of NO for renal perfusion and the change in renal NO bioavailability due to arterial hypertension and its modification by antihypertensive therapy. SUMMARY: NO critically contributes to renal perfusion. There is evidence of reduced but also of unchanged NO bioavailability in the renal vasculature of patients with arterial hypertension both from protein expression and functional studies. In particular, drugs interacting with the renin-angiotensin-aldosterone system (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and aldosterone antagonists) and third-generation beta blockers are promising candidates to improve renal endothelial function. It is not yet clear whether these specific effects translate into prevention of nephrosclerosis.

Antihypertensive Agents↗

PubMed1998

University of Miami Division of Clinical Pharmacology Therapeutic Rounds: ischemic renal disease.

Ischemic renal disease (IRD) is defined as a significant reduction in glomerular filtration rate and/or loss of renal parenchyma caused by hemodynamically significant renal artery stenosis. IRD is a common and often overlooked clinical entity that presents in the setting of extrarenal arteriosclerotic vascular disease in older individuals with azotemia. IRD is an important cause of chronic renal failure and end-stage renal disease (ESRD), and many patients with a presumed diagnosis of hypertensive nephrosclerosis may actually have undiagnosed ischemic nephropathy as the cause of their ESRD. The primary reason for establishing the diagnosis of IRD is the hope that correction of a renal artery stenosis will lead to improvement of renal function or a delay in progression to ESRD. There are six typical clinical settings in which the clinician could suspect IRD: acute renal failure caused by the treatment of hypertension, especially with angiotensin-converting enzyme inhibitors; progressive azotemia in a patient with known renovascular hypertension; acute pulmonary edema superimposed on poorly controlled hypertension and renal failure; progressive azotemia in an elderly patient with refractory or severe hypertension; progressive azotemia in an elderly patient with evidence of atherosclerotic disease; and unexplained progressive azotemia in an elderly patient. It is important for the clinician to identify IRD, because IRD represents a potentially reversible cause of chronic renal failure in a hypertensive patient.

Aged↗

PubMed2004

Development of chronic kidney disease and cardiovascular prognosis in essential hypertensive patients.

The existence of a significant percentage of treated hypertensive patients presenting a diminished renal function has been recently described. Mild renal function abnormalities are recognized as powerful predictors of cardiovascular morbidity and mortality. However, longitudinal data demonstrating this association are lacking. The objectives of this study have been analysis of the evolution of GFR, assessed as creatinine clearance (CrCl), during long-term follow-up of hypertensive patients and evaluation of the impact of the development of chronic kidney disease (CKD) on cardiovascular prognosis. A historical cohort of 281 patients attending our Hypertension Unit was selected according to the following criteria: essential hypertension, more than 5 yr of follow-up, and normal GFR at baseline (CrCl > 90 ml/min per 1.73 m(2)). Patients had an average follow-up of 13.2 +/- 4.8 yr. Forty-one patients (14.6%) developed CKD (CrCl < 60 ml/min per 1.73 m(2)) attributed to hypertensive nephrosclerosis. Initial serum creatinine, age, systolic BP at baseline, and average total cholesterol during follow-up were independent predictors of CKD development. Forty-nine (17.4%) of 281 patients presented a cardiovascular event during follow-up: 17 patients (40.6%) who developed CKD and 32 patients (13.3%) with preserved renal function (log rank test P < 0.001). After adjustment in a Cox multivariate analysis, age, development of CKD during follow-up, and male gender were independent predictors of the appearance of cardiovascular events. In essential hypertensive patients with normal renal function at baseline, the development of CKD during the follow-up is strongly and independently related with poor cardiovascular prognosis.

Adolescent↗

PubMed2004

Ischemic nephropathy: where are we now?

Identification and reversing the loss of kidney function beyond occlusive disease of the renal arteries poses a major clinical challenge. Recent studies indicate that atherosclerotic renal artery stenosis develops as a function of age and is commonly associated with other microvascular disease, including nephrosclerosis and diabetic nephropathy. The risks of renal artery stenosis are related both to declining kidney function and to accelerated cardiovascular disease, with increased morbidity and mortality. Newer drugs, including agents that block the renin-angiotensin system, have improved the level of BP control for renovascular hypertension. Progressive renovascular disease during medical therapy can produce refractory hypertension, congestive heart failure, and renal failure with tubulointerstitial fibrosis. Recent studies indicate a complex interplay of oxidative stress, endothelial dysfunction, and activation of fibrogenic cytokines as a result of experimental atherosclerosis and renal hypoperfusion. Advances in imaging and interventional devices offer major new opportunities to prevent progressive loss of kidney function. Recent series indicate that although 25 to 30% of patients with impaired renal function can recover glomerular filtration after revascularization, many have no apparent change in kidney function and 19 to 25% experience a significant loss of kidney function, in some cases as a result of atheroemboli. To select patients who are most likely to benefit from vascular intervention, clinicians should understand the pathophysiology of developing ischemic nephropathy and the potential hazards of revascularization in the setting of diffuse atherosclerotic disease. Further research should be directed toward identification of critical disease, regulation of fibrogenesis, and the interaction with other atherosclerotic processes.

Humans↗

PubMed2004

A comparison of iothalamate-GFR and serum creatinine-based outcomes: acceleration in the rate of GFR decline in the African American Study of Kidney Disease and Hypertension.

In renal clinical trials, both slope-based and time-to-event renal outcomes have been used. These outcomes are typically based on estimates of GFR obtained using creatinine or iothalamate GFR (iGFR). The African American Study of Kidney Disease and Hypertension (AASK) was a trial in 1094 African Americans with hypertensive nephrosclerosis, which examined the effects of two levels of BP control and three antihypertensive regimens. This study compared the effects of the AASK interventions on outcomes based on serum creatinine with corresponding outcomes based on iGFR using 9742 matched pairs of iGFR and serum creatinine measurements. The iGFR-based outcomes included (1) a time-to-event composite outcome including a 50% GFR decline, ESRD, or death; (2) a composite outcome including a 50% GFR decline or ESRD; (3) mean decline in GFR in the first 3 mo after randomization (acute slope); (4) mean decline in GFR starting 3 mo after randomization (chronic slope); and (5) mean decline in GFR from baseline (total slope). The corresponding creatinine-based outcomes were (1) a composite of doubling of serum creatinine, ESRD, or death and (2) a composite of doubling of serum creatinine or ESRD and acute, chronic, and total slopes defined by the mean change in estimated GFR (eGFR), where eGFR was estimated from a regression equation for GFR depending primarily on serum creatinine and developed in AASK enrollees. Mean changes in iGFR and eGFR were also compared under extended models that allowed for the possibility that the rate of GFR decline may change over time during the chronic phase. an apparent acceleration in rate of decline of renal function over time was found. Subtle differences were observed between effects of the interventions on some of the creatinine and iGFR slope-based outcomes, but the main conclusions of the trial were similar for the serum creatinine and iothalamate-based measurements. This has important implications for the design of clinical trials with renal outcomes.

Adolescent↗

PubMed2004

Crosslink breakers: a new approach to cardiovascular therapy.

PURPOSE OF REVIEW: Advanced glycation end-products accumulate on body proteins with aging, and their formation is greatly enhanced with rising plasma glucose level. Advanced glycation end-products bond together and, consequently, increase protein crosslinking. In the circulatory system, increased collagen crosslinking caused by advanced glycation end-products increases cardiovascular stiffness as well as the risk for cardiovascular morbidity and mortality. A breaker of advanced glycation end-products-related crosslinks, ALT-711, has been recently discovered. This review summarizes the latest evidence that breaking collagen crosslinks may be an efficient new therapeutic approach to the adverse cardiovascular and renal consequences of aging and diabetes. RECENT FINDINGS: The results of recent studies clearly demonstrated that ALT-711, a breaker of advanced glycation end-products-related protein crosslinks, ameliorated the adverse cardiovascular and renal changes associated with aging, diabetes, and hypertension. In diabetic animals, ALT-711 improved left ventricular function, decreased ventricular collagen content and improved its solubility, reduced aortic stiffness, ameliorated diabetic nephrosclerosis, and improved renal function. In older spontaneously hypertensive rats, it reduced left ventricular mass and collagen content, reduced proteinuria, and extended survival. The results of recent studies also indicated that the effects of crosslinks breakers may be mediated in part via reduction in oxidative stress and profibrotic cytokines. SUMMARY: The results of experimental studies and one clinical trial have clearly established the usefulness of ALT-711 in the therapy of the cardiovascular and renal disorders associated with aging, diabetes, and hypertension. Thus, breaking advanced glycation end-products-related collagen crosslinks has emerged as a new approach to cardiovascular therapy.

Aging↗

PubMed2005

Increased renal resistive index in atherosclerosis and diabetic nephropathy assessed by Doppler sonography.

OBJECTIVE: The renal resistive index (RI) and pulsatility index (PI), measured using Doppler ultrasonography, reflect intrarenal vascular resistance. We evaluated the relationship between these indices and pulse wave velocity (PWV), a measure of arterial stiffness, which reflects atherosclerosis, and determined whether renal RI and PI differ depending on the underlying renal disease. METHODS: A total of 245 inpatients with or without renal impairment who underwent ultrasonographic assessment of the renal artery were enrolled in the study. Patients with renal artery stenosis or severe renal failure (serum creatinine>or=6 mg/dl) were excluded from the study. RESULTS: In univariate analysis, the RI and PI of the main renal arteries and the interlobar arteries were significantly correlated with PWV. Multivariate analyses showed that PWV was independently associated with the RI of the main renal arteries (P<0.01, R=0.256). Patients with a creatinine level less than 3 mg/dl were divided into a control group without renal diseases and three groups with different underlying renal diseases: diabetic nephropathy, chronic glomerulonephritis, and nephrosclerosis. The RI and PI of the main renal arteries and the interlobar arteries were significantly higher in patients with diabetic nephropathy than in the other three groups, even after adjusting for multiple variables, including creatinine clearance. CONCLUSION: These results suggest that the increased RI of the renal arteries is associated with the severity of systemic atherosclerosis. Furthermore, the intrarenal vascular resistance differs depending on the underlying renal disease, and appears to increase to a greater extent in diabetic nephropathy.

Adult↗

PubMed2004

Prevention of renal fibrosis by spironolactone in mice with complete unilateral ureteral obstruction.

PURPOSE: Recent data suggest that aldosterone directly mediates cardiac fibrosis and hypertensive nephrosclerosis. We conducted experiments to determine whether administration of spironolactone, a mineralocorticoid receptor antagonist, reduced renal fibrosis in an experimental model of obstructive uropathy. MATERIALS AND METHODS: Complete unilateral ureteral obstruction (UUO) was created surgically in 8 to 10-week-old male C57BL/6 mice by placing sutures around the right ureter. Spironolactone (50 mg/kg/daily) or 1% dimethyl sulfoxide vehicle was administered by subcutaneous injection for 1 to 2 weeks, and renal fibrosis was assessed by measuring trichrome staining and type I collagen deposition in the kidney. RESULTS: UUO lasting 1 week was associated with minimal parenchymal damage and spironolactone had no demonstrable effect. In contrast, administration of the mineralocorticoid antagonist (8 mice) for a 2-week period significantly reduced renal fibrosis in the obstructed kidney, compared to mice given the dimethyl sulfoxide vehicle (9). The beneficial effect of spironolactone treatment was not associated with any changes in serum potassium or aldosterone concentration, or urinary concentrations of sodium or potassium. CONCLUSIONS: Administration of spironolactone reduced renal fibrosis in mice with UUO. These findings suggest that clinical trials are warranted to determine the efficacy of aldosterone antagonists in conjunction with angiotensin converting enzyme inhibitors and/or angiotensin receptor blockers as renoprotective agents in patients with obstructive uropathy.

Animals↗

PubMed2005

Administration-time-dependent effects of antihypertensive treatment on the circadian pattern of blood pressure.

PURPOSE OF REVIEW: Many studies show that the extent of the nocturnal blood-pressure decline is deterministic of cardiovascular injury and risk. Accordingly, there is growing interest in how to tailor the treatment of hypertensive patients according to their circadian blood-pressure pattern. RECENT FINDINGS: Differences in efficacy depending on the time of day of drug administration lead to differences in effects of antihypertensive drugs on the nocturnal decline relative to the diurnal mean of blood pressure. Thus, bedtime dosing with nifedipine gastrointestinal therapeutic system (GITS) is more effective than morning dosing, while also reducing significantly secondary effects. Bedtime administration of trandolapril results in a safe and effective means of controlling morning blood pressure without inducing excessive reduction nocturnally. The dose-response curve, therapeutic coverage, and efficacy of doxazosin GITS are all markedly dependent on the circadian time of drug administration. Moreover, valsartan administration at bedtime as opposed to upon wakening results in improved day/night blood-pressure ratio, a significant increase in the percentage of controlled patients after treatment, and a significant reduction in urinary albumin excretion. SUMMARY: Nocturnal hypertension increases one's risk of cardiovascular and cerebrovascular events, nephrosclerosis, and progression to end-stage kidney failure in renal patients. Normalization of the circadian blood-pressure pattern is considered an important clinical goal of pharmacotherapy because it may slow the advance of renal injury. Chronotherapy provides a means of individualizing treatment of hypertension according to the circadian blood-pressure profile of each patient, and constitutes a new option in optimizing blood-pressure control and reducing risk.

Adrenergic alpha-Antagonists↗

PubMed2006

Primary hypertension and nephropathy.

PURPOSE OF REVIEW: The relationship between primary hypertension (formerly called essential hypertension) and hypertension-associated chronic kidney disease is complex and poorly understood. The strong association between hypertension-associated chronic kidney disease and cardiovascular disease supports the existence of common mediators. We will review data indicating common mediating mechanisms for cardiovascular disease and chronic kidney disease in primary hypertension. RECENT FINDINGS: Chronic kidney disease develops in primary hypertension due to local and systemic inflammatory mediators that cause endothelial injury. This injury is an important early step in the development of hypertension-associated vasculopathy that causes nephron ischemia with nephrosclerosis. Similar mechanisms mediate endothelial injury in cardiovascular disease and its progression. Subjects with primary hypertension at increased risk for chronic kidney disease are at higher risk for cardiovascular disease, the major cause of mortality in primary hypertension. SUMMARY: Primary hypertension is a modifiable risk factor for both cardiovascular disease and chronic kidney disease. Better understanding of how primary hypertension leads to these outcomes might help in the development of pharmacologic strategies that retard and/or prevent chronic kidney disease in primary hypertension. Because of the strong association between cardiovascular disease and chronic kidney disease in primary hypertension, this improved understanding will likely lead to better therapies to hinder the development and/or progression of cardiovascular disease, in addition to its benefits in preventing hypertension-associated chronic kidney disease.

Albuminuria↗