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PubMed1996

Growth characteristics of cells cultured from two murine models of polycystic kidney disease.

Polycystic kidney disease (PKD) is characterized by multiple renal cysts that are lined by epithelium and filled with fluid. PKD may result from one of a number of factors, either inherited or environmental. In this study, we have compared two mouse models in which PKD results from a genetic cause. In the C57BL/6J-cpk model, the mutated gene is unknown. In the other model, an SV40 large T antigen transgene causes renal cysts. We examined cultured cells from the kidneys of these mouse models, comparing growth characteristics. Although several features of PKD lead one to expect that the epithelial cells lining the cysts would have an increased rate of proliferation in culture, we found that they did not. The implications of these findings are discussed.

Animals↗
PubMed2007

Stabilization of glomerular filtration rate in advanced chronic kidney disease: a two-year follow-up of a cohort of chronic kidney disease patients stages 4 and 5.

This study examines whether stabilization of the glomerular filtration rate (GFR) is possible in patients with advanced chronic kidney disease (CKD), managed in a CKD clinic. A cohort of 82 patients with stages 4 and 5 CKD was followed for a period of 2 years after initiation of erythropoietin for anemia to determine the GFR and the frequency of primary outcomes (dialysis, transplantation, or death). GFR, calculated by the abbreviated Modification of Diet in Renal Disease formula, was determined every 3 months. After 24 months, 35 subjects (43%) developed a primary outcome. Controlled for other risk factors, the risk of having a primary outcome increased 19.7% for every unit that the GFR decreased (95% confidence interval [CI], 11.9%-26.8%, P < .001) and decreased 21.7% for every unit that the hemoglobin increased (95% CI, 0.5%-38.4%, P < .001). Blacks had a 3.1 times higher risk (95% CI, 1.4-6.9, P = .006) of developing a primary outcome than other ethnicities. In subjects who did not develop primary outcomes (n = 47 or 57%), GFR remained unchanged (19.5 +/- 9.1 at the end of the study v 20.8 +/- 5.3 mL/min/1.73 m(2) at baseline, P = .16). The standardized mortality rate was 4.75 and 9.77 per 100 person-year for stages 4 and 5, respectively. We conclude that stabilization of GFR over a 2-year period can be achieved in many patients with advanced CKD treated with erythropoietin in a CKD clinic. Although the precise reason for the stabilization of GFR cannot be elucidated from this study, our data are "proof of concept" that CKD outcomes can be improved in a CKD clinic setting.

Adult↗
PubMedDate not supplied

Polycystic kidney disease: an unrecognized emerging infectious disease?

Polycystic kidney disease (PKD) is one of the most common genetic diseases in humans. We contend that it may be an emerging infectious disease and/or microbial toxicosis in a vulnerable human subpopulation. Use of a differential activation protocol for the Limulus amebocyte lysate (LAL) assay showed bacterial endotoxin and fungal (1-->3)-beta-D-glucans in cyst fluids from human kidneys with PKD. Fatty acid analysis of cyst fluid confirmed the presence of 3-hydroxy fatty acids characteristic of endotoxin. Tissue and cyst fluid from three PKD patients were examined for fungal components. Serologic tests showed Fusarium, Aspergillus, and Candida antigens. IgE, but not IgG, reactive with Fusarium and Candida were also detected in cyst fluid. Fungal DNA was detected in kidney tissue and cyst fluid from these three PKD patients, but not in healthy human kidney tissue. We examine the intertwined nature of the actions of endotoxin and fungal components, sphingolipid biology in PKD, the structure of PKD gene products, infections, and integrity of gut function to establish a mechanistic hypothesis for microbial provocation of human cystic disease. Proof of this hypothesis will require identification of the microbes and microbial components involved and multifaceted studies of PKD cell biology.

Communicable Diseases↗
PubMed2005

Bone disease in patients with chronic kidney disease under conservative management.

CONTEXT AND OBJECTIVE: Few studies have focused on bone disease in patients with chronic kidney disease under conservative treatment. The objective was to evaluate bone disease in patients with chronic kidney disease. DESIGN AND SETTING: Case series, at the Nephrology Division, Hospital Universitário Pedro Ernesto. METHODS: 131 patients with creatinine clearance from 10 to 60 ml/min/1.73 m(2) were followed up for at least one year. Serum creatinine, albumin, calcium, phosphorus, alkaline phosphatase, total CO2 (tCO2), intact parathyroid hormone (iPTH), and alkaline phosphatase were measured. Creatinine clearance was calculated from 24-hour urine creatinine measurements and protein ingestion estimates from urea assays. RESULTS: Patients presenting creatinine clearance < 30 ml/min/1.73 m(2) had higher iPTH values, but normal serum levels for calcium, phosphorus, alkaline phosphatase and tCO2. Patients presenting iPTH values of twice the normal upper limit (144 pg/ml) showed lower tCO2 values. Bone alkaline phosphatase was evaluated in 37 patients with creatinine clearance < 30 ml/min/1.73 m(2), showing correlation with alkaline phosphatase but not with parathyroid hormone. Bone biopsy on nine patients with creatinine clearance < 30 ml/min/1.73 m(2) and iPTH > 144 pg/ml showed osteitis fibrosa (4), mild lesion (4) and high turnover (1). CONCLUSION: The present data suggest the importance of early control for iPTH and metabolic acidosis, among patients under conservative management for chronic kidney disease, in order to prevent complications related to bone disease.

Absorptiometry, Photon↗
PubMed1998

Potassium citrate/citric acid intake improves renal function in rats with polycystic kidney disease.

Polycystic kidney disease (PKD) has been shown to be exacerbated by acidosis or a low potassium intake, and there is evidence that administration of alkali might have a beneficial effect. This study determined whether ingestion of potassium citrate and citric acid would ameliorate PKD. Healthy normal and heterozygous littermate Han:SPRD rats with autosomal dominant PKD were provided with either tap water or 55 mM K3citrate/67 mM citric acid solution (KCitr) to drink starting at the age of 1 mo. Renal clearance measurements and histologic assessments were performed when the rats were 3 mo old. KCitr intake did not affect body weight or urine flow, but completely prevented the decline in GFR found in untreated rats with PKD. In rats that drank tap water, left kidney GFR averaged (in microliter/min per 100 g body wt) 503 +/- 78 (n = 9) in normal animals and 242 +/- 56 (n = 6) in rats with PKD. In rats that drank KCitr, GFR averaged 562 +/- 123 (n = 7) in normal animals and 534 +/- 103 (n = 7) in rats with PKD. Kidneys of rats with PKD were approximately double normal size. KCitr treatment did not affect kidney size, but led to fewer interstitial abnormalities and smaller cysts in cystic kidneys. KCitr ingestion led to a significantly lower (P < 0.001) plasma [K+] in rats with PKD (3.3 +/- 0.2 versus 4.1 +/- 0.2 mEq/L in rats on tap water). Chronic KCitr intake in the young heterozygous Han:SPRD rat with PKD yields a modest improvement of kidney histology and a dramatic improvement in GFR. The mechanism of action of KCitr and the long-term effects of this treatment on renal structure and function in PKD deserve further study.

Analysis of Variance↗
PubMed2006

Detection of chronic kidney disease in patients with or at increased risk of cardiovascular disease: a science advisory from the American Heart Association Kidney And Cardiovascular Disease Council; the Councils on High Blood Pressure Research, Cardiovascular Disease in the Young, and Epidemiology and Prevention; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: developed in collaboration with the National Kidney Foundation.

Chronic kidney disease (CKD) occurs commonly in patients with cardiovascular disease. In addition, CKD is a risk factor for the development and progression of cardiovascular disease. In this advisory, we present recommendations for the detection of CKD in patients with cardiovascular disease. CKD can be reliably detected with the combined use of the Modification of Diet in Renal Disease equation to estimate glomerular filtration rate and a sensitive test to detect microalbuminuria. All patients with cardiovascular disease should be screened for evidence of kidney disease with these two determinations.

American Hospital Association↗
PubMed1984

Multiple forms of alanine aminopeptidase, alkaline phosphatase and gamma-glutamyltransferase in urine of healthy persons, patients suffering from kidney diseases and patients with kidney transplants.

The catalytic activities of alanine aminopeptidase, alkaline phosphatase and gamma-glutamyltransferase were determined in the soluble and particulate fractions of urine, after ultracentrifugation. In healthy adults the fractional catalytic activities in the supernatants were 0.53, 0.56 and 0.24, respectively. Nearly the same proportions were found in children. In patients suffering from chronic kidney diseases there was a tendency for the proportion of catalytic activity in the soluble fraction to increase. However, the separation into the multiple forms gave no higher diagnostic reliability than the determination of total catalytic activity of the respective enzymes. The determination of multiple forms has no clinical significance in the detection of rejection episodes in renal transplant recipients.

Adult↗
PubMed1998

Renal endothelin system in polycystic kidney disease.

Polycystic kidney disease (PKD) is characterized by interstitial fibrosis and formation of renal cysts. Interestingly, interstitial fibrosis and renal cyst formation were also seen in human endothelin-1 (ET-1) transgenic mice. This study, therefore, analyzes the tissue distribution of ET-1, the tissue concentrations of ET-1, as well as the expression of ET receptor subtypes in the kidneys of a rat model of PKD: Han:SPRD rats. Six-week-old heterozygous (cy/+) and homozygous (cy/cy), as well as 6-mo-old heterozygous (cy/+) Han:SPRD rats and the corresponding age-matched Sprague Dawley littermates (SD) (+/+) were analyzed. Furthermore, the acute effects of the mixed (A/B) endothelin receptor antagonist bosentan on hemodynamic and renal function were investigated in 6-mo-old, conscious, chronically instrumented (cy/+) rats. The kidneys of affected rats showed significantly elevated tissue levels of ET-1 compared with age-matched controls (3.5 +/- 0.3-fold in young cy/cy rats, P < 0.01; 1.4 +/- 0.2-fold in young cy/+ rats, P < 0.01; 6.2 +/- 0.4-fold in old cy/+ rats, P < 0.001) due to a highly increased ET-1 synthesis within the epithelial cells of the cysts. Analyzing tissue sections from patients with typical autosomal dominant PKD demonstrated a high ET-1 expression within the epithelial cells of the cysts as well. Scatchard analysis revealed a markedly decreased ETA and ETB receptor density in all groups of affected rats. The acute blockade of both endothelin receptor subtypes using bosentan in 6-mo-old heterozygous PKD rats led to a significant decrease in mean arterial BP (MAP) (-19.7 +/- 2.1 mmHg, P < 0.05) and GFR (-41 +/- 5%, P < 0.005). Renal blood flow (RBF) was significantly increased (+2.1 +/- 0.5 ml/min, P < 0.05) after bosentan, whereas bosentan had no effect on MAP, GFR, and RBF in age-matched controls. These data show that the paracrine renal endothelin system is activated in PKD and participates in the regulation of MAP, GFR, RBF, and possibly contributes to renal cyst formation and fibrosis.

Analysis of Variance↗
PubMed1990

Autosomal dominant polycystic kidney disease: a linkage evaluation of heterogeneity in Italy. Italian Collaborative Group on Polycystic Kidney Disease.

A survey of 29 families with Adult Polycystic Kidney Disease (ADPKD) was performed to evaluate the genetic heterogeneity of the disease in Italy. The approach was through the linkage between the disease and 2 polymorphic DNA fragments as detected by the probes 3'HVR and 24.1. Linkage between the polymorphic markers and the disease was confirmed, with the following lod scores: between 3'HVR and ADPKD1 = 12.974 at theta = 0.02; between 24.1 and ADPKD = 1.716 at theta = 0.07; between 3'HVR and 24.1 = 2.738 at theta = 0.09. No evidence of significant genetic heterogeneity in the examined Italian regions was detected.

Genes, Dominant↗
PubMed1989

[Pathogenesis of anemia due to kidney disease].

Several factors contribute to the pathogenesis of anemia due to renal failure. Hypoproliferation of red cell progenitors may be caused partially by an inhibitory effect of some 'uremic toxins' whose existence certainly is very controversial. Iron deficiency due to gastrointestinal and dialysis-related blood losses and occasionally aluminum intoxication may interfere with the maturation of the erythron. Moderate hemolysis with shortening of red cell survival to some 50% of normal may be an additional factor. The main cause of anemia is, however, inadequate production of erythropoietin by the diseased kidney. This latter factor has now become amenable to treatment.

Anemia↗
PubMed2006

Mechanisms of Disease: autosomal dominant and recessive polycystic kidney diseases.

Autosomal dominant polycystic kidney disease and autosomal recessive polycystic kidney disease are the best known of a large family of inherited diseases characterized by the development of renal cysts of tubular epithelial cell origin. Autosomal dominant and recessive polycystic kidney diseases have overlapping but distinct pathogeneses. Identification of the causative mutated genes and elucidation of the function of their encoded proteins is shedding new light on the mechanisms that underlie tubular epithelial cell differentiation. This review summarizes recent literature on the role of primary cilia, intracellular calcium homeostasis, and signaling involving Wnt, cyclic AMP and Ras/MAPK, in the pathogenesis of polycystic kidney disease. Improved understanding of pathogenesis and the availability of animal models orthologous to the human diseases provide an excellent opportunity for the development of pathophysiology-based therapies. Some of these have proven effective in preclinical studies, and clinical trials have begun.

Animals↗
PubMed2005

The goals of comprehensive and integrated disease state management for diabetic kidney-disease patients.

Diabetes, cardiovascular disease, and chronic kidney disease present many challenges to clinicians as separate disease entities. Management and optimization of care of diabetic kidney-disease patients requires a proactive and integrated approach for all 3 disease states. To optimize the assessment, monitoring, and intervention in this population, comprehensive and integrated disease state management medical care plans must be established. Medical nutrition therapy is another key component that must be coordinated with these disease-state management medical care plans. Coordination of integrated disease-state management and medical nutrition therapy for diabetes, cardiovascular disease, and chronic kidney disease will help to improve patient outcomes and allow for a proactive approach to the identification, prevention, and management of potential disease-state complications. Several programs and guidelines have been established to accomplish these goals: the K/DOQI Clinical Practice Guidelines, the American Diabetes Association Standards of Medical Care for Diabetes (developed by the American Diabetes Association, the National Institute of Diabetes and Digestive Kidney Diseases, and the Centers for Disease Control-Diabetes Foundation), the National Diabetes Education Program, and the National Cholesterol Education Program. The multidisciplinary medical care team assumes an integral role in the success and implementation of this integrated approach as well as the empowerment of the patient in their own care.

Cardiovascular Diseases↗
PubMed2005

[From gene to disease; PKHD1 and recessive polycystic kidney disease].

Autosomal recessive polycystic kidney disease (ARPKD) is a severe form of polycystic kidney disease characterised by enlarged kidneys and congenital hepatic fibrosis. The disease has an incidence of 1:7000-:20,000 and is caused by mutations in the PKHD1 gene, which under normal conditions produces the protein fibrocystin, also named polyductin. This protein may be a transmembrane receptor or ligand that plays a role in collecting duct and biliary differentiation. The major site of expression is the primary cilium, and in particular the basal body of the cilium, underlining a link between aberrant cilial function and cystogenesis. Prenatal diagnostics is possible using DNA analysis or ultrasonography.

Humans↗
PubMed2005

Strategies to retard the progression of chronic kidney disease.

Chronic kidney disease (CKD) is a common and, in advanced cases, highly morbid disorder. The most severe form of CKD is end-stage renal disease (ESRD), in which the patient requires some form of renal replacement therapy to survive. The increasing incidence, prevalence, and costs of ESRD are major national health care concerns; interventions that may prevent or slow the progression of CKD towards ESRD are extremely important and the focus of this article.

Anemia↗
PubMed2004

Polycystic kidney syndrome in New Zealand White rabbits resembling human polycystic kidney disease.

BACKGROUND: Cystic kidney diseases are an important cause of morbidity and mortality in humans. Small animal models are needed to more fully explore the complex expression patterns and pathobiology of this group of heritable diseases. METHODS: We performed a 15-year retrospective analysis of cases in our laboratory animal diagnostic archives to determine the prevalence of cystic kidney disease in New Zealand White rabbits. RESULTS: Out of 203 records with documented renal histopathology, we identified and defined 7 cases of polycystic kidney syndrome (PKS) by 3 morphologic criteria: (1) cysts or microcysts derived from tubules, glomeruli, or both; (2) loose mesenchymal expansion of cortical and/or medullary interstitium; and (3) irregular thickening, thinning, and splitting of basement membranes. PKS was associated with hypercalcemia and hypercreatinemia (P < 0.01), and arterial mineralization resembling Mönckeberg's medial calcific sclerosis. In the liver, mild chronic cholangitis with cholangiodysplasia and fibrosis was common. Anorexia and lethargy were the clinical signs most often reported. CONCLUSION: Clinicopathologic characterization of PKS in New Zealand White rabbits revealed similarities to both autosomal-dominant and autosomal-recessive polycystic kidney diseases of humans. Awareness of polycystic kidney syndrome in New Zealand White rabbits will allow investigators to avoid using affected animals in unrelated renal research. Prospective studies are needed to define the underlying cause(s) of polycystic kidney syndrome in New Zealand White rabbits, which may be an important new small animal model of human cystic kidney diseases.

Animals↗