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PubMed1997

Immunization with bacterial antigens: bacterial kidney disease.

Bacterial kidney disease has consistently resisted attempts to control it by prophylactic immunisation. Although successful vaccines have been produced to a number of Gram-negative fish pathogens, the relatively simple method used in these cases have not been successful with Renibacterium salmoninarum. A more circumspect and thorough knowledge of the biological function of R. salmoninarum antigens must be obtained. Also required is a more precise understanding of the role of regional immunity in effective prophylaxis. Aspects of R. salmoninarum's biology provide a provocative challenge to the vaccinologist. Its residence in, and apparent commandeering of the macrophage, indicate that a vigorous cell-mediated response will probably be required to generate protective immunity. Its most biologically potent secreted product, p57, appears to be an aggressin. Further, p57 has the capability of frustrating immunoprophylaxis by either misdirecting the immune response, or by preventing its induction. Many immunization studies have used injection immunization and challenge protocols. It now appears that alternative routes of immunization which had been considered less protective (i.e. oral immunization) may not only be more efficacious, but may be the only route that does not lead to a misdirected and possibly pathological immune response. Also, the general reliance on serum antibodies as the only means to assess immunity is fraught with difficulties, particularly with pathogens such as R. salmoninarum. Recent advances in the analysis of cellular immunity will be a great aid in the design of future vaccines.

Animals↗

PubMed1995

The pathogenesis of polycystic kidney disease.

Polycystic kidney disease (PKD) is a genetic or acquired disorder characterized by progressive distention of multiple tubular segments and manifested by fluid accumulation, growth of non-neoplastic epithelial cells and remodeling of the extracellular matrix resulting ultimately in some degree of renal functional impairment, with the potential for regression following removal of the inductive agent(s). It is due to an aberration of one or more factors regulating tubular morphogenesis. Human PKD can pursue a rapid course with renal failure occurring perinatally (infantile PKD) or an indolent course without renal failure developing during the life of the individual (adult PKD). Human acquired PKD develops in atrophic and scarred end-stage kidneys with non-cystic forms of renal disease. Cell proliferation, fluid secretion, impaired cell-cell and cell-matrix interaction, defective function of the Golgi apparatus, cell undifferentiation, and an abnormal matrix have been implicated in the pathogenesis of PKD based on clinical and experimental studies. Under normal conditions, the dynamic turnover of tubular epithelia and matrices are tightly regulated to maintain tubular morphology. The basic defect in PKD is tubular dysmorphogenesis. Our finding indicates that the principal phenotypic features of autosomal dominant PKD (ADPKD) are altered structure and function of the Golgi complex, altered structure and composition of the matrix and cell undifferentiation, all of which are probably interrelated. If the gene product of the ADPKD 1 gene results in a defective matrix, the abnormal Golgi function and cell differentiation may be due to faulty matrix-cell communication.

Animals↗

PubMed2005

Traditional and nontraditional cardiovascular risk factors in chronic kidney disease.

Chronic kidney disease (CKD) is public health problem, with as many as 20 million individuals affected in the United States. Patients with CKD should be considered in the highest-risk group for development of cardiovascular disease (CVD), and aggressive treatment of traditional and nontraditional risk factors should be instituted. Additional randomized controlled trials are urgently needed to evaluate potential treatments in this population. This article focuses attention on the major modifiable cardiovascular risk factors in CKD.

Cardiovascular Diseases↗

PubMed2005

Piecing together the evidence on anemia: the link between chronic kidney disease and cardiovascular disease.

Chronic kidney disease (CKD) is now accepted as an independent cardiovascular disease (CVD)-risk state, regardless of its underlying cause. Anemia is a common feature of CKD, particularly in end-stage renal disease. Anemia is also independently associated with poorer outcomes in a wide variety of CVD states, including congestive heart failure and coronary artery disease. Anemia appears to act as an independent mortality multiplier when hemoglobin levels drop below 12 g/dL. With the independent and profound contribution of both CKD and anemia to cardiovascular mortality and morbidity, understanding the pathophysiologic links among these disease states is important. In addition, it is hoped that treatments currently under active investigation and geared specifically to attenuate the cardiovascular risk associated with anemia and CKD, such as erythropoietin therapy, will improve outcomes. This article reviews the evidence for an association among CKD, anemia, and CVD.

Anemia↗

PubMedDate not supplied

[Can cardiovascular calcifications be prevented in chronic kidney disease?].

Chronic kidney disease, with special regard to hemodialysis patients, develop frequent and widespread cardiac and vascular calcifications. In the heart calcifications are mainly located in the coronary arteries and in the valvular structures. There is a strict relation between cardiovascular mortality in CKD and the extent of cardiac and vascular calcifications. Therefore it is important to evaluate the causes of extraskeletal calcifications for the evaluation of the possibility of prevention. The importance of hyperphosphatemia, of hypercalcemia and of the increased CAxP product as a cause of cardiac calcification has been clearly underlined. However the mechanism of calcification, initially considered a physico-chemical precipitation, has been investigated with the conclusion that the process is mediated by cellular differentiation and production of factors favoring mineralization in the extracellular milieu. Increased serum phosphate levels are able to induce a transformation of vascular smooth muscle cells into osteoblast-like cells, able to produce factors known to be pro-mineralizing agents in the bone tissue. Further studies have revealed the importance of a number of inhibitors of calcification of cardiovascular structures, like Fetuin-A, MGP, Osteopontin, Osteoprotegerin. Therefore at present the calcification process of vascular tissue is considered to be linked to a balance between inducers and inhibitors of calcium-phosphate deposits. Prevention of cardiac calcifications is at present mainly based of optimal control of serum phosphate and reduction of calcium load through the use of non-calcium containing phosphate binders. Treatment with statins for prevention and treatment of atherosclerosis is also an important means of decreasing the size and number of atherosclerotic plaques, where a portion of the calcification process develops.

Calcinosis↗

PubMed1996

Role of lactosylceramide and MAP kinase in the proliferation of proximal tubular cells in human polycystic kidney disease.

Polycystic kidney disease (PKD) is a common genetic disease characterized by the proliferation of epithelial cells, formation of cysts, and the progression of renal deficiency. We have investigated a possible role of glycosphingolipids in the proliferation of human kidney cells in this disease. The levels of glucosylceramide and lactosylceramide and the activity of glucosylceramide synthase (GlcT-1) and lactosylceramide synthase (GalT-2) were elevated 2-fold and 3-fold, respectively, in the PKD tissue compared to control. Lactosylceramide, but not glucosylceramide (10 microM) derived from PKD exerted a 4-fold stimulation in the proliferation of these cells. However, at a concentration of 40 microM, lactosylceramide and glucosylceramide both stimulated cell proliferation on the order of 10-fold and 2.5-fold, respectively, as compared to control. This phenomenon may be due to the enrichment of lactosylceramide containing shorter chain fatty acids (C16:0-C18:0). Lactosylceramide, but not glucosylceramide exerted a time-dependent stimulation in the phosphorylation of mitogen-activated protein kinase (p44 MAPK) in normal human kidney proximal tubular cells. Moreover, the kidneys and cultured cells from the PKD patients contained higher levels of the p44 MAPK as compared to normal human kidneys. In sum, our studies indicate that lactosylceramide present in the PKD kidney may stimulate cell proliferation via activation of the p44 MAPK, and contribute to the pathophysiology in this disease.

Adult↗

PubMed1994

Autosomal recessive polycystic kidney disease does not map to the second gene locus for autosomal dominant polycystic kidney disease on chromosome 4.

Linkage analysis in 19 families with autosomal recessive polycystic kidney disease (ARPKD) has shown that ARPKD is not linked to the recently assigned second gene locus for autosomal dominant polycystic kidney disease (ADPKD) on chromosome 4q (PKD2). Thus, there is strong evidence that ADPKD and ARPKD have different gene loci.

Chromosome Mapping↗

PubMedDate not supplied

In vitro and in vivo assessment of intraintestinal bacteriotherapy in chronic kidney disease.

Chronic kidney disease may progress to end-stage renal disease, which requires dialysis or kidney transplantation. No generally applicable therapies to slow progression of renal disease are available. Bacteriotherapy affords a promising approach to mitigate uremic intoxication by ingestion of live microbes able to catabolize uremic solutes in the gut. The present study evaluates the nonpathogenic soil-borne alkalophilic urease-positive bacterium Sporosarcina pasteurii (Sp) as a potential urea-targeted component for such "enteric dialysis" formulation. Data presented herein suggest that Sp survives through exposure to gastric juice retaining the ability to hydrolyze urea. In vitro, 10 cfu (colony forming units) of Sp removed from 21 +/- 4.7 mg to 228 +/- 6.7 mg urea per hour, depending on pH, urea concentration, and nutrient availability. Beneficial effects of Sp on fermentation parameters in the intestine were demonstrated in vitro in the Simulator of the Human Intestinal Microbial Ecosystem (SHIME) inoculated with fecal microbiota. Enumeration of marker organisms suggested that presence of Sp does not disturb microbial community of the SHIME. Additionally, a pilot study in 5/6th nephrectomized rats fed 10 cfu of live Sp daily throughout the study demonstrated that the tested regimen reduced blood urea-nitrogen levels and significantly prolonged the lifespan of uremic animals.

Animals↗

PubMed1989

Molecular genetics and polycystic kidney diseases.

Polycystic kidney diseases (PKDs) comprise a group of common disorders, inherited as a monofactorial trait, usually dominant but sometimes recessive. The origin and mechanism of these diseases are unknown. Molecular genetics has now provided the means to seek the diseased gene(s), however, and, once found, to unravel the protein sequence and ultimately to understand the pathophysiology of these disorders.

Chromosome Mapping↗

PubMed2000

[Kidney disease and insulin resistance--clinical impact of thiazolidinedione compounds for kidney disease].

The thiazolidinedione compounds are well known hypoglycemic agents via increasing insulin-sensitivity. Herein, we provide the possibility that thiazolidinedione compounds could be useful for renal dysfunction through mechanism dependent or independent of its insulin-sensitizing action. In type 2 diabetes, troglitazone could reduce urinary albumin-creatinine ratio compared to metformin. Furthermore, we have shown that troglitazone was able to prevent diabetic glomerular dysfunction through inhibition of diacylglycerol-protein kinase C-extracellular signal-regulated kinase pathway in type 1 diabetic rats. Thus, thiazolidinediones might be effective agents for treating insulin-resistant diabetes as well as diabetes-induced kidney disease.

Animals↗

PubMed1992

Attenuated expression of epithelial cell adhesion molecules in murine polycystic kidney disease.

Polycystic kidney disease is an inherited disorder of parenchymal structure that leads to renal failure. Cysts begin as focal dilations in proximal tubules and collecting ducts, giving rise to cyst walls lined by a phenotypically disturbed epithelium that expresses dysfunctional transport and matrix proteins. We used an mRNA search protocol to probe efficiently for tissue-specific disturbances that might underlie the formation of cysts. This search assessed the relative abundance of transcripts encoding a variety of growth factors (transforming growth factor-beta 1, interleukin-6, tumor necrosis factor, and endothelin-1), structural proteins (collagen IV, nidogen, fibronectin, and laminins A and B1), and cell adhesion molecules (CAMs; E-cadherin, N-CAM, laminin receptor, and fibronectin receptor) in the cystic kidneys of cpk/cpk mice and uncovered a previously unrecognized early reduction in mRNA encoding N-CAM (54%) and E-cadherin (56%) (n = 5; P less than 0.001). Levels of transcripts for growth factors, structural proteins, and for fibronectin and laminin receptors in normal and cystic kidneys were generally similar. The reduction in transcripts for N-CAM and E-cadherin in kidneys from cystic mice was not observed in autologous liver. The immunofluorescent staining of cystic kidneys confirmed that the decrease in N-CAM and E-cadherin was generally confined to regions abundant in developing cystic epithelium. The presence of both N-CAM and E-cadherin appears to guide the sequential differentiation and polarization of normal renal epithelium, and their attenuated expression in the kidney of cpk/cpk mice may be a material factor contributing to the pathogenesis of cyst formation.

Animals↗

PubMed2003

Kidney-specific inactivation of the KIF3A subunit of kinesin-II inhibits renal ciliogenesis and produces polycystic kidney disease.

Polycystic kidney disease (PKD) is the most common genetic cause of renal failure in humans. Several proteins that are encoded by genes associated with PKD have recently been identified in primary cilia in renal tubular epithelia. These findings have suggested that abnormalities in cilia formation and function may play a role in the pathogenesis of PKD. To directly determine whether cilia are essential to maintain tubular integrity, we conditionally inactivated KIF3A, a subunit of kinesin-II that is essential for cilia formation, in renal epithelia. Constitutive inactivation of KIF3A produces abnormalities of left-right axis determination and embryonic lethality. Here we show that tissue-specific inactivation of KIF3A in renal tubular epithelial cells results in viable offspring with normal-appearing kidneys at birth. Cysts begin to develop in the kidney at postnatal day 5 and cause renal failure by postnatal day 21. The cyst epithelial cells lack primary cilia and exhibit increased proliferation and apoptosis, apical mislocalization of the epidermal growth factor receptor, increased expression of beta-catenin and c-Myc, and inhibition of p21(CIP1). These results demonstrate that the absence of renal cilia produces both the clinical and cell biological findings associated with PKD. Most generally, the phenotype of Kif3a mutant mice suggests a role for primary cilia in the maintenance of lumen-forming epithelial differentiation.

Animals↗

PubMed1981

Early diagnosis of polycystic kidney disease.

Polycystic kidney disease is the most prevalent hereditary renal disorder, accounting for over 5 percent of patients on chronic hemodialysis. Early diagnosis can aid in family planning, and "preventive therapy" may prolong useful life and defer dialysis. Intravenous pyelography with nephrotomography has been the standard procedure for definitive diagnosis, but ultrasonography, radionuclide scanning and computerized tomography have become increasingly useful. Ultrasonography is particularly valuable because it is free of radiation hazards. Impaired urinary concentrating ability is a frequent early sign of the disorder.

Adult↗

PubMed2005

Management of peripheral arterial disease in chronic kidney disease.

PAD has been overlooked in many epidemiologic studies evaluating cardiovascular risk associated with renal disease. Conversely, CKD has not been evaluated as a potential risk factor in epidemiologic studies of PAD. PAD, however,seems to be more prevalent among patients with even moderate CKD than in the general population and is most common among chronic dialysis patients, one third or more of whom have a low ABI. Patients with CKD also seem to be at increased risk for developing claudication and for requiring surgical intervention for lower extremity PAD. Furthermore, even moderate CKD seems to be a risk factor for postoperative death and complications after both lower extremity amputation and revascularization procedures. Conversely, even asymptomatic PAD seems to be a risk factor for death among dialysis patients. In the general population, statins, antiplatelet agents (particularly clopidogrel), antihypertensive agents, and ACE inhibitors all have a proven benefit in reducing cardiovascular events in patients with PAD and in some instances may also reduce PAD events. Available evidence suggests that patients with CKD also experience cardio-vascular risk reduction with statin and ACE-inhibitor therapy, but these therapies have not been shown to reduce PAD events specifically in patients with CKD. Further studies are needed to identify interventions that can specifically reduce the incidence of PAD complications in patientswith CKD. Although it is clear that mortality and complication rates after both lower extremity amputation and revascularization are increased in patients with even moderate CKD, currently available observational studies do not provide clear guidance for surgical decision making in CKD patients with limb-threatening ischemia. Further studies are needed to evaluate the risksand benefits of amputation over revascularizationamong patients with CKD and to investigatereasons for the high mortality associated with these procedures in this patient group. Further studies are also needed to measure the impact of CKD on care processes for PAD with the goal of identifying target areas for improvement.

Chronic Disease↗

PubMed2002

Hemorheological investigations in patients with polycystic kidney disease.

Polycystic kidney disease (PKD) is associated with an increased incidence of hypertension and cardiovascular abnormalities. As hemorheology is an important hemodynamic determinant and may contribute to vasculopathies we measured whole blood viscosity and red blood cell (RBC) and plasma rheological factors in 38 patients with PKD and compared this data with similar measurements in age- and sex-matched healthy controls. Renal function was assessed by plasma creatinine concentration. Analysis of the data showed that the PKD group had a significant reduction in mean hematocrit and an increase in mean plasma viscosity and mean plasma fibrinogen concentration. Intrinsic RBC rheology assessed by standardised viscosity measurements was impaired in patients with PKD compared to control subjects. The changes in plasma and RBC rheology did not however result in increased whole blood viscosity in the patients with PKD due to the reduction in hematocrit level. Correlation analyses demonstrated a significant relationship between increased plasma creatinine concentration and lower hematocrit, decreased whole blood viscosity and impaired RBC deformability but not with increased plasma viscosity or plasma fibrinogen concentration. This study shows that although PKD is associated with mild abnormalities in plasma rheology and intrinsic RBC rheology these changes are offset by a reduction in hematocrit. The changes in RBC rheological determinants in PKD appeared to be related to the degree of renal impairment.

Adult↗

PubMed2004

Evaluation of eHealth web sites for patients with chronic kidney disease.

BACKGROUND: Chronic kidney disease (CKD) affects up to 19.2 million Americans, and untreated kidney disease can progress to kidney failure. Patient education is an important part of slowing disease progression, but the ability of health professionals to provide this education is limited by time constraints. To date, there have been no systematic evaluations of CKD eHealth Web sites. METHODS: Seven nonproprietary and 4 proprietary Web sites geared toward educating patients with CKD were identified by using the Internet to search for the terms "chronic kidney disease," "kidney disease," and "chronic renal failure." Web sites were evaluated according to (1) compliance with the principles of the Health on the Net (HON) Foundation Code of Conduct and (2) reading grade level. RESULTS: Nonproprietary sites were in compliance with an average of 5.2 principles, with a range of 3 to 8. Average compliance of proprietary Web sites with the HON Code of Conduct principles was 3.12, with a range of 2 to 4 (P = 0.021). Of nonproprietary Web sites, average reading grade level assessed by the Fry Readability Scale was greater than grade 14, with a range from grade 11 through graduate school. Of proprietary sites, average readability was grade 11, with a range from grades 7 through 16 (P = 0.575). CONCLUSION: The Internet has the potential to be a very powerful educational tool for patients with CKD. However, many easily accessed CKD public health Web sites do not comply with accepted standards for health Web sites and are written using language beyond the general public's reading comprehension.

Adult↗

PubMed2004

The prevalence of nontraditional risk factors for coronary heart disease in patients with chronic kidney disease.

BACKGROUND: Risk for coronary heart disease is high among patients with chronic kidney disease. OBJECTIVE: To compare the prevalence of low apolipoprotein A1 levels and elevated apolipoprotein B, plasma fibrinogen, lipoprotein(a), homocysteine, and C-reactive protein levels by estimated glomerular filtration rate (GFR). DESIGN: Cross-sectional study. SETTING: Third National Health and Nutrition Examination survey. PARTICIPANTS: 12 547, 3180, and 744 persons with estimated GFRs of at least 90, 60 to 89, or less than 60 mL/min per 1.73 m2, respectively, who were at least 18 years of age. MEASUREMENTS: Chronic kidney disease was defined as an estimated GFR of less than 60 mL/min per 1.73 m2 based on the abbreviated Modification of Diet in Renal Disease formula. RESULTS: After standardization for age, race or ethnicity, and sex, lower estimated GFR (> or =90, 60 to 89, or <60 mL/min per 1.73 m2) was associated with lower average levels of apolipoprotein A1 (1.44, 1.43, and 1.35 g/L) and higher levels of apolipoprotein B (1.03, 1.06, and 1.08 g/L), plasma fibrinogen (8.43, 8.44, and 9.53 micromol/L), homocysteine (8.5, 10.0, and 13.2 micromol/L), and C-reactive protein (3.0, 2.9, and 3.9 mg/L) (P < 0.05 for all values). The multivariate-adjusted odds ratios of an apolipoprotein A1 level of less than 1.2 g/L, a serum lipoprotein(a) level of at least 1.61 micromol/L (> or =45.3 mg/dL), a plasma fibrinogen level of at least 10.35 micromol/L, a serum homocysteine level of at least 15 micromol/L, and a C-reactive protein level of at least 10.0 mg/L for participants with chronic kidney disease compared with those with a GFR of at least 90 mL/min per 1.73 m2 or greater were 1.92 (95% CI, 1.02 to 3.63), 1.82 (CI, 1.06 to 3.13), 1.74 (CI, 1.35 to 2.24), 8.23 (CI, 5.00 to 13.6), and 1.93 (CI, 1.33 to 2.81), respectively. CONCLUSIONS: Levels of apolipoprotein A1 are decreased and levels of homocysteine, lipoprotein(a), fibrinogen, and C-reactive protein are increased among patients with chronic kidney disease.

Adult↗

PubMed1995

Cilazapril delays progression of hypertension and uremia in rat polycystic kidney disease.

Polycystic kidney disease (PKD) is the fourth most common cause of end-stage renal disease and is a common cause of hypertension and associated vascular morbidity. Activity of the renin angiotensin system has been identified as a major component of hypertension and altered fluid and electrolyte physiology in PKD. Activity of this pathway also has been proposed as a potential modulator of structural change in both tubules and the interstitium of the kidney. Cilazapril is a long-acting angiotensin-converting enzyme inhibitor that has been effective in producing vascular remodelling in hypertensive vascular disease. We undertook a study to determine whether therapy with cilazapril would modify the expression of PKD in the Han:SPRD-cy rat, a model of autosomal dominant PKD that closely resembles human disease. Male rats were treated for 4 months, starting at 1 month of age. Control animals were hypertensive by 3 months of age, whereas treated animals were noted to be hypertensive only at the exit assessment (P < 0.001 at 3 months, P = 0.005 at 5 months). At 5 months of age, cilazapril-treated animals had modest but statistically significant reductions in serum creatinine (mean, 1.77 mg/dL v 1.97 mg/dL; P = 0.0006) and morphometrically assessed cyst volume (mean, 0.32 mL v 0.67 mL; P = 0.036). Cilazapril is an effective treatment for hypertension in this model of progressive renal disease and may have benefits beyond the prevention of cardiovascular morbidity.

Angiotensin-Converting Enzyme Inhibitors↗