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PubMed1995

Circulating type VI collagen and undulin, in patients with kidney diseases, after kidney transplantation and on hemodialysis.

Chronic kidney diseases are characterized by alterations in connective tissue turnover resulting in fibrosis. We measured circulating peptides related to type VI collagen and undulin in serum and urine of 125 patients with various kidney diseases, on chronic hemodialysis and after kidney transplantation. Using a double-armed ELISA technique (median, 95% CI), normal serum concentrations for type VI collagen were 50 ng/ml [46-63] with no type VI collagen detectable in urine. Normal values for undulin were 215 ng/ml [207-241] in serum and 240 micrograms/d [223-284] in urine. The serum concentrations of undulin were most significantly (477 ng/mg [358-737]) increased in 18 hemodialysis patients. A significant increase (330 ng/ml [306-368]) was also observed in patients with various kidney diseases not requiring dialysis. No differences were found between the various forms of glomerulonephritis, interstitial nephritis and other kidney diagnoses. Although very low in normals (1.16 ml/min [1.05-1.27]) renal undulin clearance was even significantly lower in patients with kidney diseases (0.5 ml/min [0.4-0.6]). Serum concentrations for undulin were in the normal range in the direct postoperative phase after kidney transplantation (207 ng/ml [167-306]), whereas in kidney transplant out-patient levels were elevated to 425 ng/ml [357-563]. There was a slight but significant correlation between serum undulin and creatinine values and between renal undulin clearance and creatinine clearance. Values of serum type VI collagen increased in analogy to those of undulin. We conclude, that type VI collagen and undulin are novel serum parameters of renal extracellular matrix turnover that merit further exploration in patients with chronic kidney diseases.

Adolescent↗
PubMed1991

Chromium-induced kidney disease.

Kidney disease is often cited as one of the adverse effects of chromium, yet chronic renal disease due to occupational or environmental exposure to chromium has not yet been reported. Occasional cases of acute tubular necrosis (ATN) following massive absorption of chromate have been described. Chromate-induced ATN has been extensively studied in experimental animals following parenteral administration of large doses of potassium chromate (hexavalent) (15 mg/kg body weight). The chromate is selectively accumulated in the convoluted proximal tubule where necrosis occurs. An adverse long-term effect of low-dose chromium exposure on the kidneys is suggested by reports of low molecular weight (LMW) proteinuria in chromium workers. Excessive urinary excretion of beta 2-microglobulin, a specific proximal tubule brush border protein, and retinol-binding protein has been reported among chrome platers and welders. However, LMW proteinuria occurs after a variety of physiologic stresses, is usually reversible, and cannot by itself be considered evidence of chronic renal disease. Chromate-induced ATN and LMW proteinuria in chromium workers, nevertheless, raise the possibility that low-level, long-term exposure may produce persistent renal injury. The absence of evidence of chromate-induced exposure may produce persistent renal injury. The absence of evidence of chromate-induced chronic renal disease cannot be interpreted as evidence of the absence of such injury. Rather, it must be recognized that no prospective cohort or case-control study of the delayed renal effects of low-level, long-term exposure to chromium has been published.

Animals↗
PubMed2003

Lillian Jean Kaplan International Prize for advancement in the understanding of polycystic kidney disease. Understanding polycystic kidney disease: a systems biology approach.

Understanding polycystic kidney disease: A systems biology approach. Fluid secretion was discovered in the mammalian nephron in the early 1970s upon a chance observation. This finding aroused interest in the possibility that a similar process might be involved in the filling of renal epithelial cysts. A research strategy was formulated to understand the life cycle of human renal cysts using a systems biology approach. A not-for-profit foundation was begun to increase the number of researchers in the United States and abroad working on the polycystic kidney disease (PKD) problem. Primary outcomes related to PKD include (1). explication of the transport mechanisms underlying the transepithelial secretion of chloride, sodium and fluid, and the regulation of that secretion by cyclic adenosine monophosphate (AMP); (2). the discovery that cyclic AMP stimulates the proliferation of cyst epithelial cells through activation of of B-Raf and the mitogen-activated protein (MAP) kinase pathway; and (3). the discovery that normal medullary collecting ducts secrete solutes and fluid under the control of cyclic AMP. The Polycystic Kidney Disease Foundation has become an international leader in promoting the research of these disorders and is a strong advocate for increased translation of fundamental laboratory discoveries to the care of the millions of patients with PKD.

Animals↗
PubMed2003

Anaemia, cardiovascular disease and kidney disease: integrating new knowledge in 2002.

PURPOSE OF REVIEW: The present review assesses recent publications, from 2001 until the present, which address the relationship between cardiovascular disease (CVD) and anaemia in patients with chronic kidney disease. RECENT FINDINGS: Insights from the recently published basic science literature have helped to place findings from clinical studies into a new context, and thereby assist us to understand and further explore the complex relationship between haemoglobin level and survival in chronic kidney disease. The effects of erythropoietin molecules and the presence of receptors in vascular endothelium, myocardium and other tissues are described. Both observational and interventional clinical studies are examined, and limitations in the methodology and statistical analysis of clinical studies are emphasized, but are given context within the body of literature preceding the past year's publications. SUMMARY: Data suggest that development of CVD in patients with kidney disease is multifactorial. Several factors associated with CVD are also associated with anaemia, thereby making causal arguments for the role of anaemia in CVD and survival difficult. Arguments are made for the importance of prevention of anaemia and of individualizing therapeutic goals for its treatment. Well designed prospective studies with both CVD events and mortality as outcomes, and with enrollment beginning before the start of dialysis, are essential if we are to determine the optimal therapeutic strategies.

Anemia↗
PubMed2005

Cinacalcet HCl: a novel treatment for secondary hyperparathyroidism in stage 5 chronic kidney disease.

BACKGROUND: Chronic kidney disease (CKD) alters the regulation of calcium and phosphate homeostasis, leading to secondary hyperparathyroidism, metabolic bone disease, soft tissue calcifications, and other metabolic derangements that have a significant impact on morbidity and mortality. The parathyroid gland is the central organ responsible for regulating these adaptive responses. Suppression of parathyroid hormone (PTH) secretion, hypertrophy, and hyperplasia are a major goal of treatment of CKD. METHODS: Current literature was reviewed and combined with the author's experience to address a number of issues regarding the optimal treatment of secondary hyperparathyroidism in hemodialysis patients. RESULTS: The calcium sensing receptor (CASR) is the most important factor regulating parathyroid gland function, and allosteric modulators of CASR, called calcimimetics, provide a novel drug therapy to suppress PTH secretion. The current use of active vitamin D analogues to suppress PTH is often limited by hypercalcemia and hyperphosphatemia. Clinical trials of cinacalcet HCl, the first calcimimetic to be approved for treatment of secondary hyperparathyroidism in CKD, have demonstrated suppression of circulating PTH levels without increments in the calcium-phosphorus (Ca x P) product, making it easier to achieve the stringent management guidelines proposed for subjects with CKD by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI). CONCLUSION: The management of disordered calcium and phosphate homeostasis in CKD patients is evolving based on our knowledge of the major importance of the calcium sensing receptor (CASR) in controlling parathyroid gland function and the potent actions of calcimimetics to target CASR. The purpose of this presentation is to provide an overview of the role of the CASR in regulation of parathyroid gland function, to examine the mechanisms whereby calcimimetics target the CASR, and to review the clinical trials that support the use of cinacalcet HCl for the treatment of secondary hyperparathyroidism in stage 5 chronic kidney disease (CKD).

Chronic Disease↗
PubMed2004

Ethical implications of ethnic disparities in chronic kidney disease and kidney transplantation.

Chronic kidney disease (CKD) is a major epidemic in underserved and minority populations largely due to excess rates of hypertensive and diabetic kidney disease. Multiple complex socioeconomic barriers to early diagnosis and optimal therapies as well as delayed referral for kidney transplantation have created disparities in CKD care provided to ethnic minorities. Disparities exist in wait list time and kidney transplant rates for Native Americans and blacks, independent of insurance status. Moreover, independent of genetic matching, long-term transplant outcomes in blacks remain significantly lower than all other ethnic groups, suggesting that poorly understood social factors contribute to these survival differences. The existence of these disparities raises ethical concerns of equity and social justice in terms of the allocation of scarce resources. Although current changes in allocation policies will improve some disparities, more efforts are ultimately needed to improve access to care and the overall health and survival for all individuals at risk for CKD, independent of their race, ethnicity, or socioeconomic status.

Black or African American↗
PubMed2005

Multiple risk factor intervention in chronic kidney disease: management of cardiac disease in chronic kidney disease patients.

This article describes the relationship between CVD and CKD, the current state of knowledge regarding medical interventions, and underscores the importance of attending to both CVD and kidney disease aspects in each individual. The burden of cardiac disease in CKD patients is high with severe LVH, dilated cardiomyopathy and coronary artery disease occurring frequently. This predisposes to congestive heart failure, angina, myocardial infarction, and death. Multiple risk factors for cardiac disease exist and include hypertension, diabetes, smoking, anemia, abnormal calcium and phosphate metabolism, inflammation, and LVH. The efficacy of risk factor intervention has not been established in these populations, although there is good evidence for good blood pressure control, partial correction of anemia, treatment of dyslipidemia, cessation of tobacco use, correction of divalent abnormalities, and aspirin us. Appropriate use of ACE inhibitors, beta-blockers, and statins should be encouraged.

Cardiovascular Diseases↗
PubMed2000

Development of subscales from the symptoms/problems and effects of kidney disease scales of the kidney disease quality of life instrument.

BACKGROUND: The Kidney Disease Quality of Life Instrument (KDQOL) was developed to provide clinicians with a comprehensive assessment of the important domains of health-related quality of life (HRQOL) for patients with end-stage renal disease who are undergoing hemodialysis. OBJECTIVE: The purpose of this study was to develop subscales from the 55 items comprising the Symptoms/Problems and Effects of Kidney Disease scales of the KDQOL and to measure the internal consistency reliability of these subscales. METHODS: The 55 items from the Symptoms/Problems and Effects of Kidney Disease scales were arranged into substantively meaningful clusters using an affinity mapping procedure. The resulting subscales were assessed for internal consistency reliability using data from a sample of 165 individuals with kidney disease who had completed the KDQOL. RESULTS: Eleven multi-item subscales were identified: pain, psychological dependency, cognitive functioning, social functioning, dialysis-related symptoms, cardiopulmonary symptoms, sleep, energy, cramps, diet, and appetite. Four items (clotting or other problems with access site, high blood pressure, numbness in hands or feet, and blurred vision) were not included in any of these subscales. Internal consistency reliability estimates for the 11 subscales ranged from 0.66 to 0.92. These subscales correlated with the scales from the 36-Item Short-Form Health Survey as hypothesized (ie, corresponding pain, energy, and social functioning scales had the highest correlations). In addition, several subscales were significantly associated, as hypothesized, with other variables such as the number of disability days. CONCLUSIONS: The results of this study further support the reliability and validity of the KDQOL. The 11 subscales identified yield more detailed information on the HRQOL of patients with kidney disease and provide a basis for specific improvements in the quality of care delivered to these patients.

Adult↗
PubMed2002

Effects of antioxidants on kidney disease.

Kidney mesangial cells (MCs) and vascular smooth muscle cells (VSMCs) are closely related in terms of origin, microscopic anatomy, histochemistry, and contractility. This relationship suggests a similarity between kidney glomerular sclerosis and atherosclerosis. Vitamin E appears beneficial in the prevention and treatment of coronary disease and also inhibits the proliferation of VSMCs in vitro. We used vitamin E and probucol to treat glomerular sclerosis and MC-proliferative glomerulonephritis (GN) in two animal models of glomerular disease. Using rats, a remnant kidney model accelerated with hyperlipidemia was employed to reflect progressive glomerular sclerosis leading to chronic renal failure, and an anti-thymocyte serum treatment was used to model acute MC-proliferative GN. Supplemental dietary antioxidants suppress MC proliferation and glomerular sclerosis in models of glomerular disease in rats. These results suggest that treatment with antioxidants may be a promising intervention to prevent progression of kidney disease.

Animals↗
PubMed1996

Isolated polycystic liver disease as a distinct genetic disease, unlinked to polycystic kidney disease 1 and polycystic kidney disease 2.

Polycystic liver disease (PLD) is proven to occur either sporadically or in association with autosomal dominant polycystic kidney disease (ADPKD), whereas the existence of an isolated (i.e., without any kidney cyst) familial form is disputed. We describe a family with definitely isolated PLD transmitted through three generations and exclude the linkage of the disease to the genetic markers of PKD1 and PKD2, the two main loci responsible for ADPKD. These findings strongly support the existence of PLD as a genetic disease distinct from the known forms of ADPKD.

Cysts↗
PubMed1989

Glomerular localization of type III collagen in human kidney disease.

Kidney specimens taken from normal humans and patients with various renal diseases were examined by immunofluorescent and immunoelectron microscopy using a monoclonal antibody to the alpha 1 chain of type III collagen. Indirect immunofluorescent staining revealed that intraglomerular localization of type III collagen antigen in 41 of 66 patients, while it was absent from the glomeruli of normal human kidneys. Type III collagen was found within the mesangium of 22 patients with various types of renal diseases, and was distributed in a focal and segmental manner in most of the cases. Mesangial localization of the collagen correlated with the increase in the mesangial matrix. Type III collagen was also present in the vascular pole, crescents (particularly in the organizing phase) and sclerosed glomeruli. Immunoelectron microscopy using pre-embedding and post-embedding techniques confirmed the above observations. These findings indicate that type III collagen participates in mesangial expansion, crescent organization, and glomerulosclerosis.

Antibodies↗
PubMed2004

Mechanism of albuminuria associated with cardiovascular disease and kidney disease.

The major underlying factors associated with tissue damage and fibrosis in cardiovascular and kidney disease are the up-regulation and action of growth factors such as transforming growth factor-beta (TGF-beta) and cytokines produced in response to changes in systemic factors, particularly blood pressure or hyperglycemia. This study identifies the relationship of elevated levels of TGF-beta to increased levels of intact albumin in the urine (micro- and macroalbuminuria). This mechanism may be directly linked to the effect of TGF-beta on albumin uptake and the lysosomal breakdown of filtered albumin by proximal tubular cells prior to excretion.

Albuminuria↗
PubMed2006

Anemia and cardiovascular and kidney disease.

PURPOSE OF REVIEW: The joint occurrence of cardiovascular disease, kidney disease and anemia has been termed the 'cardio-renal-anemia syndrome'. This review will examine each of these relationships as they pertain to coronary heart disease. RECENT FINDINGS: Important contributions from the recent literature included observations suggesting that African-Americans with chronic kidney disease and no previous history of cardiovascular disease were more likely than caucasians to have incident cardiovascular disease than caucasians with chronic kidney disease but that this difference did not apply to risk of recurrent cardiovascular disease. Recent reports have brought attention to a continued lack of clinical trials evidence to support anemia treatment for cardioprotection, further concern that higher hemoglobin levels may increase cardiovascular risk and evidence that anemia and kidney function interact to increase risk for coronary heart disease. Finally, additional observational studies and small clinical trials continue to support a role of anemia treatment in protection of residual kidney function, although a recent meta-analysis failed to demonstrate a conclusive benefit of erythropoietin treatment on progressive kidney disease. SUMMARY: The cardio-renal-anemia syndrome is a set of complex and interrelated phenomena that are poorly understood. Current evidence is insufficient to demonstrate a conclusive benefit of treatment with erythropoietin on risk of cardiovascular disease or progression of kidney disease. Future research is needed to further clarify these issues.

Adult↗
PubMed1980

Von Hippel-Lindau disease simulating polycystic kidney disease.

Polycystic kidney disease and the renal manifestations of von Hippel-Lindau disease have much in common. Making the distinction between these two diseases is important. There is a strong association of renal cell carcinoma with von Hippel-Lindau disease, whereas renal cell carcinoma is rare in polycystic kidney disease. Furthermore, the many extrarenal manifestations of von Hippel-Lindau disease are serious and can be fatal while those of polycystic kidney disease are generally benign. Early diagnosis of the lesions of von Hippel-Lindau disease could lead to effective surgical treatment and prevent death. A case of von Hippel-Lindau disease is presented which was incorrectly diagnosed as polycystic kidney disease for sixteen years. The case is instructive in that the possibility of making the correct diagnosis prior to the patient's terminal illness was only through careful assessment of the family. The case is also remarkable in that the patient suffered from progressive renal failure requiring hemodialysis, which has not been associated previously with von Hippel-Lindau disease.

Adult↗
PubMed2005

Definition and classification of chronic kidney disease: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO).

Chronic kidney disease (CKD) is a worldwide public health problem, with adverse outcomes of kidney failure, cardiovascular disease (CVD), and premature death. A simple definition and classification of kidney disease is necessary for international development and implementation of clinical practice guidelines. Kidney Disease: Improving Global Outcomes (KDIGO) conducted a survey and sponsored a controversies conference to (1) provide a clear understanding to both the nephrology and nonnephrology communities of the evidence base for the definition and classification recommended by Kidney Disease Quality Outcome Initiative (K/DOQI), (2) develop global consensus for the adoption of a simple definition and classification system, and (3) identify a collaborative research agenda and plan that would improve the evidence base and facilitate implementation of the definition and classification of CKD. The K/DOQI definition and classification were accepted, with clarifications. CKD is defined as kidney damage or glomerular filtration rate (GFR) <60 mL/min/1.73 m(2) for 3 months or more, irrespective of cause. Kidney damage in many kidney diseases can be ascertained by the presence of albuminuria, defined as albumin-to-creatinine ratio >30 mg/g in two of three spot urine specimens. GFR can be estimated from calibrated serum creatinine and estimating equations, such as the Modification of Diet in Renal Disease (MDRD) Study equation or the Cockcroft-Gault formula. Kidney disease severity is classified into five stages according to the level of GFR. Kidney disease treatment by dialysis and transplantation should be noted. Simple, uniform classifications of CKD by cause and by risks for kidney disease progression and CVD should be developed.

Albuminuria↗