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PubMed2002

Cardiovascular disease and the kidney. Tracking a killer in chronic kidney disease.

The interlinking of CVD with CKD is undeniable. CVD accounts for more than 50% of all morbidity and mortality in patients with kidney disease who have undergone renal replacement therapy, and CVD is also prevalent in patients with mild and moderately severe kidney disease. To help address the elevated risks of these patients, primary care physicians need to maintain vigilance in (1) identifying patients who have CKD and (2) implementing strategies for reducing the prevalence of CVD in this population. It is essential that patients be screened for relatively mild kidney disease by measurement of serum creatinine and urine microalbumin and by calculation of the glomerular filtration rate in mL/min/1.73 m2 using equations based on serum creatinine. Rigorous assessment of conventional risk factors, including dyslipidemia, hypertension, and diabetes, is also necessary to prevent the poor outcomes currently observed in persons with CKD. Routine use of ACE inhibitors and aspirin is encouraged in all patients with CKD, and strict glycemic and blood pressure control is recommended for optimal outcomes. In addition, patients should be screened and treated for risk factors particularly associated with kidney disease and CVD morbidity and mortality, including anemia, hyperphosphatemia, and hyperparathyroidism. Finally, physicians should be careful to avoid therapeutic nihilism in patients with kidney disease; those at highest risk of CVD are likely to receive the greatest benefit from cardiovascular therapies.

Cardiovascular Diseases↗
PubMed2005

Renal insulin resistance syndrome, adiponectin and cardiovascular events in patients with kidney disease: the mild and moderate kidney disease study.

The relationship among insulin resistance, adiponectin, and cardiovascular (CV) morbidity in patients with mild and moderate kidney disease was investigated. Insulin sensitivity (Homeostasis Model Assessment of Insulin Resistance [HOMA-IR]) and adiponectin plasma levels were assessed in 227 nondiabetic renal patients at different degrees of renal dysfunction and in 76 healthy subjects of similar age and gender distribution and body mass index. In renal patients, association with prevalent CV events was evaluated, and incident CV events were evaluated in a prospective study. HOMA-IR was markedly higher in patients than in healthy subjects (3.59 +/- 3.55 versus 1.39 +/- 0.51; P < 0.01). In renal patients, HOMA-IR was significantly correlated with body mass index (r = 0.477; P < 0.01), triglycerides (r = 0.384; P < 0.01), adiponectin plasma levels (r = -0.253; P < 0.01), and age (r = 0.164; P < 0.05), but not with renal function (GFR by iod-thalamate clearance). Patients with previous CV events were significantly older, had higher HOMA-IR and serum triglycerides, and had lower adiponectin plasma levels (all P < 0.05). Logistic regression analysis revealed age (P < 0.001) and adiponectin (P < 0.002) as independent variables related to prevalent CV events. In the prospective study, median follow-up was 54 mo. Patients who experienced CV events had significantly higher serum glucose and lower adiponectin plasma levels (both P < 0.05). In patients with chronic kidney diseases, a syndrome of insulin resistance is present even in the earliest stage of renal dysfunction, and several components of this syndrome are associated with CV events. Moreover, hypoadiponectinemia is a novel putative CV risk factor in patients with mild and moderate renal failure.

Adiponectin↗
PubMed2004

[Treatment of bone disease in chronic kidney disease and in renal transplant recipients under K/DOQI clinical practice guidelines].

The National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (K/DOQI) provides evidence based clinical practice guidelines developed for all phases of kidney disease and related complications, from diagnosis to monitoring and management. Bone disease sets in during the early stages of Chronic Kidney Disease (CKD). Bone disease is observed in almost patients with chronic renal failure and after renal transplantation. Hyperparathyroid (high turnover) bone disease in patients with chronic renal failure is found most frequently followed by mixed osteodystrophy, low-turn over bone disease, and osteomalasia. Ninety to one hundred percent of kidney transplant patients have histological evidence of osteodystrophy and osteopenia (reduction of bone mass) following renal transplantation. Furthermore, osteoporosis is also appeared in many renal transplant recipients. After renal transplantation, renal osteodystrophy generally improves but bone mineral density (BMD) often worsens. When renal bone disease is assessed using a combination of biochemical markers, histology and bone densitometry, early intervention and carefully effective therapies might be reduced the morbidity associated with these common problems.

Bone Density↗
PubMed1997

Autosomal dominant polycystic kidney disease in a kidney transplant population.

AIM: To define specific manifestations of autosomal dominant polycystic kidney disease in kidney transplant patients. METHODS: Of 874 consecutive first renal transplant patients 1985-1993, 114 (13%) had autosomal dominant polycystic kidney disease (ADPKD). Mean age was 53 +/- 8 years, 62% were men, and 83% received cadaveric kidneys. Control patients were matched for sex, age and donor type. Median follow-up time was 63 months. One patient was lost to follow-up. Medical records before and after transplantation were reviewed. RESULTS: Survival of patients and grafts was similar in ADPKD patients and controls. Twenty-five ADPKD patients died, four of causes not seen in the controls; two aortic aneurysms, one urothelial cancer, one colon perforation. Four more ADPKD patients but no control had diverticulitis (P = 0.03), two with perforation. Cardiovascular morbidity was not increased. Eight patients had subarachnoidal haemorrhage before transplantation and two during follow-up. Nineteen patients had undergone nephrectomy before transplantation, 11 because of voluminous kidneys, five for infection, pain or bleeding, two for suspected malignancy, one for hypertension. After transplantation, seven patients underwent nephrectomy, only one related to kidney size. During the first year, need of phlebotomy occurred in 14% of patients versus 4% of controls, P = 0.02. Urinary tract infection rates were not increased. No morbidity was related to liver cysts. CONCLUSION: The specific features of kidney transplantation to patients with ADPKD were few: enlarged kidneys, relevant only before transplantation, erythrocytosis, and as rare but serious events, diverticulitis with perforation.

Adult↗
PubMed2005

Detection and evaluation of chronic kidney disease.

Chronic kidney disease affects approximately 19 million adult Americans, and its incidence is increasing rapidly. Diabetes and hypertension are the underlying causes in most cases of chronic kidney disease. Evidence suggests that progression to kidney failure can be delayed or prevented by controlling blood sugar levels and blood pressure and by treating proteinuria. Unfortunately, chronic kidney disease often is overlooked in its earliest, most treatable stages. Guidelines from the National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (KDOQI) recommend estimating glomerular filtration rate and screening for albuminuria in patients with risk factors for chronic kidney disease, including diabetes, hypertension, systemic illnesses, age greater than 60 years, and family history of chronic kidney disease. The glomerular filtration rate, calculated by using a prediction equation, detects chronic kidney disease more accurately than does the serum creatinine level alone; the glomerular filtration rate also is used for disease staging. In most clinical situations, analysis of random urine samples to determine the albumin-creatinine or protein-creatinine ratio has replaced analysis of timed urine collections. When chronic kidney disease is detected, an attempt should be made to identify and treat the specific underlying condition(s). The KDOQI guidelines define major treatment goals for all patients with chronic kidney disease. These goals include slowing disease progression, detecting and treating complications, and managing cardiovascular risk factors. Primary care physicians have an important role in detecting chronic kidney disease early, in instituting measures to slow disease progression, and in providing timely referral to a nephrologist.

Age Distribution↗
PubMed2006

Signaling mechanism of renal fibrosis in unilateral ureteral obstructive kidney disease in ROCK1 knockout mice.

It has been shown that blockade of Rho kinase with pharmacologic inhibitors inhibits renal fibrosis. This study examined the role of Rho kinase in renal fibrosis in the unilateral ureteral obstruction (UUO) model in mice that do not express the ROCK1 gene, a critical downstream mediator of Rho GTPase. Unexpected, real-time PCR, Western blot, and immunohistochemistry demonstrated that, compared with the wild-type mice, mice with ROCK1 knockout (KO) were not protected against renal fibrosis at both the early (day 5) and late (day 10) UUO, as determined by histology and expression of both mRNA and protein levels of alpha-smooth muscle actin, collagen types I and III, and fibronectin within the diseased kidney. Then the mechanisms of loss of protective effect on renal fibrosis in ROCK1 KO mice were investigated. It is interesting that mice that lacked ROCK1 did not have altered expression of ROCK2 but significantly increased TGF-beta expression and Smad2/3 activation (phosphorylation and nuclear translocation) in the diseased kidney at day 5, which remained high at day 10 of UUO. Similarly, primary cultures of kidney fibroblasts that were obtained from both ROCK1 wild-type and KO mice showed that deletion of ROCK1 did not prevent TGF-beta-induced activation of Smad2/3 and collagen I expression. This also was observed in the presence of Rho kinase inhibitor Y-27632. Taken together, results from this study suggest that Rho/Rho kinase may not be a necessary or a central pathway for renal fibrosis in the UUO model. The interplay between the Rho/Rho kinase pathway and the Smad signaling pathway may be a key mechanism by which loss of ROCK1 does not prevent renal fibrosis in the UUO model.

Animals↗
PubMed2005

Clinical practice guidelines for bone metabolism and disease in chronic kidney disease: an overview.

The National Kidney Foundation developed and oversees the Kidney Disease Outcomes Quality Initiative, a process that develops clinical practice guidelines in nephrology. Recent guidelines address the aberrations in bone metabolism and disease that occur as a complication of chronic kidney disease. These guidelines provide, for the first time, a standard approach to the detection and management of alterations in calcium, phosphorus, and parathyroid hormone metabolism. The problems and sequelae of soft-tissue calcification are discussed, and recommendations are provided for reducing the associated morbidity and mortality.

Aluminum↗
PubMed2003

The ENOS polymorphism is not associated with severity of renal disease in polycystic kidney disease 1.

BACKGROUND: The renal phenotype in autosomal dominant polycystic kidney disease (ADPKD) is highly variable. Although genetic and allelic heterogeneity explain part of this variability, significant intrafamilial differences in time to end-stage renal disease (ESRD) indicate that genetic modifiers and the environment influence renal phenotype. Previously, a glutamic acid to aspartic acid polymorphism at residue 298 (E/D298) of the endothelial nitric oxide synthase (eNOS) gene ENOS was associated with disease severity in males with ADPKD. METHODS: We typed the E/D298 polymorphism in 215 mutation-defined polycystic kidney disease 1 (PKD1) patients from 80 families. In this population, 96 patients had ESRD, with a median time to renal failure of 53 years. RESULTS: Distribution of ENOS genotypes was 86 (40%), 106 (49.3%), and 23 (10.7%) for EE, ED, and DD, respectively. The occurrence of hypertension was not significantly different between genotypes. Kaplan-Meier renal survival analysis showed no significant difference between genotypes, with a median age to ESRD of 53 years for all genotypes in the total population and 52, 52, and 51 years (men) and 57, 53, and 55 years (women) for DD, DE, and EE, respectively. CONCLUSION: Although the D298 ENOS allele may be associated with lower vascular activity of eNOS, this did not correlate with severity of renal disease in this PKD1 population. An important difference between this study and one finding a modifying role for ENOS was the rigor in defining the PKD1 population. This study shows the importance of using mutation-characterized populations for association studies in ADPKD.

Age Factors↗
PubMed2006

Metabolic syndrome and chronic kidney disease.

Chronic kidney disease is fast becoming a worldwide epidemic. In the US, the prevalence of chronic kidney disease is 11%. Its increase in the recent years has mirrored the rising trend of obesity, hypertension and diabetes, which are all components of the metabolic syndrome. Metabolic syndrome comprises of 5 components: impaired fasting glucose, abdominal obesity, hypertriglyceridemia, hypertension and low high density lipoprotein cholesterol. While it is a well known cardiovascular risk factor in the general population, its effects in chronic kidney disease and dialysis populations has not been fully elucidated. While the number of people requiring renal replacement therapy is increasing globally, many of those with chronic kidney disease also suffer from cardiovascular morbidity and mortality. This review discusses the interaction between chronic kidney disease and metabolic syndrome, and the impact of the two on the cardiovascular risk in patients with chronic kidney disease.

Cardiovascular Diseases↗
PubMed2006

Magnetic resonance imaging in acute and chronic kidney diseases: present status.

Magnetic resonance imaging (MRI) of normal and diseased kidneys shows great promise because of the combined value of anatomical and functional information provided, as well as of specific contrast patterns that can be observed non-invasively. Multicontrast MRI is able to show infiltrative kidney disorders. Diffusion-weighted imaging can assess alterations in renal function and can suggest obstruction or inflammation when present. Due to the low nephrotoxicity, contrast-enhanced MR studies using serial dynamic enhancement with non-specific gadolinium chelates are able to provide information on glomerular filtration. Furthermore, contrast agents such as ultrasmall particles of iron oxide, specific of inflammation, should be used in the near future to detect active from quiescent involvement, both in native kidneys and renal allografts. Early results should indicate that these compounds might differentiate acute tubular necrosis from other acute nephropathies, as well as active proliferative nephropathies from chronic ones. Ongoing studies will obviously demonstrate the value of the combination of these various MRI sequences in the diagnosis of acute renal failure and chronic kidney disease.

Acute Kidney Injury↗
PubMed1997

Recent advances in the understanding of polycystic kidney disease.

Polycystic kidney disease is characterized by localized autonomous cellular proliferation, compartmentalized fluid accumulation within the cysts, and intraparenchymal fibrosis of the kidney. The clinical features include renal failure, liver cysts, and vascular and cardiac valve abnormalities. Recent developments have extended our understanding of cyst formation, fluid secretion, and the genetics of polycystic kidney disease. Two causal genes for polycystic kidney disease, PKD1 and PKD2, that are responsible for greater than 95% of cases of autosomal dominant polycystic kidney disease, have been identified and sequenced. The mechanisms of cystogenesis are being uncovered and the phenotypic features of cystic epithelial cells are being discovered. This review describes recent advances made in the molecular biology of the genetic causes of polycystic kidney disease. The mechanistic details of cystogenesis are discussed and contrasted with the paradigms that guide current experimental approaches.

Animals↗
PubMed2005

The role of statins in chronic kidney disease.

Chronic kidney disease is associated with cardiovascular event rates that are at least as high as in patients with established atherosclerotic cardiovascular disease or in those with diabetes mellitus. Chronic kidney disease is therefore considered a cardiovascular disease risk equivalent. Treatment of dyslipidemia, which is very common in this population and reflects the pattern seen in the metabolic syndrome, reduces cardiovascular events in patients with chronic kidney disease. Thus, patients with chronic kidney disease should be evaluated and treated for dyslipidemia. Dyslipidemia is a risk factor for the development of impaired kidney function. Dyslipidemia is also associated with progressive renal disease in subjects with no overt renal disease, as well as those with diabetic and nondiabetic kidney disease. Although definitive randomized controlled trials are lacking, the collective evidence suggests that treatment of dyslipidemia is associated with less decline in renal function. The use of potent statins in high doses can lead to transient proteinuria via impairment of proximal tubular receptor--mediated endocytosis, in a dose-dependent manner. Over the long term, however, the use of statins results in a reduction in proteinuria and in the rate of decline of renal function. Several large definitive trials that are currently underway to examine the safety and efficacy of statins in cardiovascular and renal protection should provide more definitive answers on the role of these drugs in this very high risk population.

Arteriosclerosis↗
PubMed2004

Insulin resistance in kidney disease patients with mild to moderate kidney disease.

BACKGROUND: Insulin resistance is a very early sign of atherosclerosis and an increased risk of cardiovascular morbidity and mortality. Insulin resistance detection by the fasting plasma insulin and glucose determination enables early detection, follow-up, treatment and the search for accelerating factors in kidney disease patients threatened by atherosclerosis. PATIENTS AND METHODS: Insulin resistance was evaluated by the Quantitative Insulin Sensitivity Check Index from fasting glucose and insulin plasma concentrations in 66 kidney disease patients with a mild to moderate decrease in kidney function. RESULTS: Forty patients were insulin sensitive and 26 suffered from insulin resistance. These groups of patients did not differ significantly in age, gender, clearance of creatinine and cholesterol concentrations. However, patients with insulin resistance suffered from increased BMI (p < 0.001), fasting plasma glucose (p < 0.01), insulin (p < 0.001) and triglyceride (p < 0.01) concentrations. Insulin resistance correlated with BMI (r = -0.417, p < 0.001) and with plasma triglycerides concentration (r = -0.307, p < 0.01). The absent relationship between insulin resistance and age (r = -0.154, NS) or creatinine clearance (r = -0.061, NS) suggests the need for screening of insulin resistance even in young patients with mild kidney function reduction. CONCLUSION: A considerable number of renal patients in the early stages of kidney function reduction suffers from insulin resistance. They need to improve their life style and take medication (i.e. antihypertensive drugs) improving insulin sensitivity and to omit medications which harm it. (Fig. 2, Tab. 1, Ref. 20.)

Female↗
PubMed1997

Polycystic kidney disease: huge kidneys, huge problems, huge progress.

Polycystic kidney disorders are more common than once appreciated, are contributors to significant morbidity, are potentially fatal and are costly to treat. In the past few years much progress has been made toward understanding the pathogenesis of renal cystic disorders. The dominantly inherited disorders are initiated by mutations within genes located in chromosomes 16 and 4 (ADPKD) that cause the kidneys to enlarge several-fold greater than normal. This enlargement is owing to the proliferation of epithelial cells in tubule segments, to the accumulation of fluid within the dilated tubule segment created by the proliferating cells, and to remodelling of the extracellular matrix. The focal beginning of ADPKD in a relatively few renal tubules suggests that the cells in the walls of cysts may reflect clonal growth and that this aberrant proliferation may be secondary to a somatic "second hit" process. The rate at which the cysts enlarge appears to depend on endocrine, paracrine and autocrine factors that drive cellular proliferation and transepithelial fluid secretion within the cysts. The presence of the renal cysts within certain kidneys appears to provoke interstitial inflammation and apoptosis that contribute to fibrosis and renal insufficiency in approximately one-half of persons with ADPKD. Why renal cysts do not cause renal failure in the other one-half of patients with polycystic kidneys is a provocative question that awaits further study.

Body Fluids↗