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PubMed1994

Renal cancer complicating acquired cystic kidney disease.

Acquired cystic kidney disease (ACKD) occurs in the setting of prolonged azotemia and is therefore common in dialysis patients. It is characterized by epithelial proliferation, and its major complication is the development of renal cancer. The incidence of renal cancer is significantly increased in ACKD patients and is probably increased overall in the ESRD population as well. Those ESRD patients with suspicious symptoms, prolonged predialysis azotemia, or a dialysis duration of longer than 3 yr, or those who are candidates for a renal transplant should be screened for ACKD. Sonography or computed tomographic scanning are useful as initial screening tools. However, although more expensive and requiring contrast administration, the contrast-enhanced computed tomographic scan is the definitive imaging procedure by which to initially evaluate a renal mass. A suspicious renal mass is a patient who is a surgical candidate is an indication for a radical nephrectomy.

Carcinoma, Papillary↗
PubMed2000

Mutations in the hepatocyte nuclear factor-1beta gene are associated with familial hypoplastic glomerulocystic kidney disease.

Familial glomerulocystic kidney disease (GCKD) is a dominantly inherited condition characterized by glomerular cysts and variable renal size and function; the molecular genetic etiology is unknown. Mutations in the gene encoding hepatocyte nuclear factor (HNF)-1beta have been associated with early-onset diabetes and nondiabetic renal disease-particularly renal cystic disease. We investigated a possible role for the HNF-1beta gene in four unrelated GCKD families and identified mutations in two families: a nonsense mutation in exon 1 (E101X) and a frameshift mutation in exon 2 (P159fsdelT). The family members with HNF-1beta gene mutations had hypoplastic GCKD and early-onset diabetes or impaired glucose tolerance. We conclude that there is genetic heterogeneity in familial GCKD and that the hypoplastic subtype is a part of the clinical spectrum of the renal cysts and diabetes syndrome that is associated with HNF-1beta mutations.

Adolescent↗
PubMed2004

Ankle brachial index independently predicts early kidney disease.

INTRODUCTION: Chronic kidney disease (CKD) and atherosclerotic cardiovascular disease (CVD) are often both present in selected populations. The independent association of early renal disease and atherosclerosis has not been studied in the general population. We hypothesized that the presence of low ankle brachial index (ABI), a surrogate measure of atherosclerotic cardiovascular disease, is associated with a low estimated glomerular filtration rate (GFR). METHODS: The study population consisted of 14,917 middle-aged black and white men and women from the Atherosclerosis Risk in Communities (ARIC) Study. An ABI<0.90 was defined as the exposure, and an estimated GFR<90 mL/min/1.73 m2 was defined as the outcome. Logistic regression analysis was performed cross-sectionally using an ABI of 1.00-1.19 as the reference, and was adjusted for the usual cardiovascular risk factors. RESULTS: The presence of an ABI<0.90 was associated with an increased odds of having an estimated GFR<90 (OR: 1.80; 95% C.I.: 1.40-2.32) compared to the reference group. After adjustment, an ABI<0.90 remained significant, and increased the odds of having an estimated GFR<90 (OR: 1.54; 95% C.I.: 1.17-2.04) compared to the reference group. The odds ratio for GFR<90 was higher among African Americans than Whites, 1.88 versus 1.36 respectively. DISCUSSION: This study gives support to the independent association of early CKD and atherosclerotic CVD. The relationship appears to be stronger among African Americans than among Whites. It will be necessary to investigate this observation more fully with prospective studies given the rising incidence of CKD.

Black or African American↗
PubMed2001

Anticipation of end stage renal disease in patients with autosomal dominant polycystic kidney disease in successive generations.

Autosomal dominant polycystic kidney disease is a disorder, which is inherited in 50% of offspring, irrelevant the sex and it has a variable clinical expressivity. Initially it was noticed that the clinical expression was interfamilial, but some studies found out that it was different. The aim of this study was to evaluate the age of onset of end-stage renal disease (ESRD) in affected parents in comparison with their offspring in successive generations. We studied 60 families of patients with autosomal dominant polycystic kidney disease (ADPKD). The diagnosis was done by echo criteria and we included only the patients for whom we knew precisely the onset of ESRD (affected parent and offspring), the sex of the parent who suffered from the disease, and offspring. We found out that the ESRD in ADPKD appears at the same age in affected parents and offspring (49,3 +/- 7,9 Vs 51,8 +/- 9,2, p = NS) irrelevant of the sex of the offspring. Patients with paternal inheritance (n = 38) were diagnosed to have ESRD earlier than their affected parents (47,9 +/- 8,3 Vs 52,2 +/- 9,2 p < 0,05), but patients with maternal inheritance had no difference (n = 22) (51,9 +/- 6,8 Vs 51,2 +/- 9,4, p = NS). In all the patients (60 couples) the survival rate was the same between affected parents and offspring (p = NS, Kaplan-Meier test), but significant differences were noticed between offspring with paternal inheritance in comparison with their parents (p < 0,05). In conclusion, we have detected that the onset of ESRD between patients with ADPKD in successive generations: a) Occurs in offspring as in their ancestors, b) anticipation was observed in 55% of couples, c) the sex of offspring does not have any relation with the renal death and d) the ESRD in patients with paternal inheritance occurs earlier in offspring than in their ancestors but not with maternal.

Adult↗
PubMed1994

Outcome measurement in kidney disease.

The effects of chronic kidney disease have been difficult to quantify using traditional measures of mortality and biological processes. New approaches to the quantification of outcomes in kidney disease are required. A wide variety of methods have become available and are now in use in some studies. Psychometric approaches, such as the Sickness Impact Profile and the Kidney Disease Questionnaire, have been shown to be responsive to change in some clinical studies. In order to estimate the cost-effectiveness of investments in kidney disease, decision theory approaches are required. We argue that these decision theory approaches should be given serious consideration for inclusion in clinical trials and in the US Renal Data System.

Decision Theory↗
PubMed2004

Medicare patients with cardiovascular disease have a high prevalence of chronic kidney disease and a high rate of progression to end-stage renal disease.

The risk of progression to ESRD among individuals with cardiovascular disease and chronic kidney disease (CKD) is not well defined. The purpose of this study was to describe the risk of ESRD among patients with cardiovascular disease. Charts were abstracted for randomly selected hospitalized Medicare beneficiaries with a diagnosis of either congestive heart failure (CHF) or acute myocardial infarction (AMI). The prevalence of CKD, based on the estimated modified diet in renal disease GFR of <60 ml/min per m2, was 60.4% of CHF patients and 51.7% of AMI patients. When compared with patients without CKD, the 30-d readmission rate was higher for CHF patients with CKD (odds ratio [OR], 1.70; 95% confidence interval [CI], 1.18 to 2.44) and for AMI patients with CKD (OR, 1.78; 95% CI, 1.17 to 2.70). CHF patients (OR, 1.62; 95% CI, 1.15 to 2.30) and AMI patients (OR, 3.10; 95% CI, 1.98 to 4.84) with CKD were more likely to die during the year after discharge from the hospital. ESRD after discharge occurred in nine of 517 patients with AMI and 24 of 640 patients with CHF. CKD increased the risk of ESRD among CHF patients (OR, 34.5; 95% CI, 4.23 to 279.43) and AMI patients (0 and 3% for those without and with CKD, respectively). At discharge, 18% of AMI patients and 21% of CHF patients with CKD were discharged with a diagnosis of renal disease. CKD is highly prevalent among patients with cardiovascular disease and is associated with increased risk of adverse outcomes, including progression to ESRD. This study suggests that opportunities may exist to improve the detection of CKD in these patients who are hospitalized with cardiovascular disease.

Acute Disease↗
PubMed2006

Molecular pathogenesis of autosomal dominant polycystic kidney disease.

Autosomal dominant polycystic kidney disease (ADPKD) is one of the commonest inherited human disorders yet remains relatively unknown to the wider medical, scientific and public audience. ADPKD is characterised by the development of bilateral enlarged kidneys containing multiple fluid-filled cysts and is a leading cause of end-stage renal failure (ESRF). ADPKD is caused by mutations in two genes: PKD1 and PKD2. The protein products of the PKD genes, polycystin-1 and polycystin-2, form a calcium-regulated, calcium-permeable ion channel. The polycystin complex is implicated in regulation of the cell cycle via multiple signal transduction pathways as well as the mechanosensory function of the renal primary cilium, an enigmatic cellular organelle whose role in normal physiology is still poorly understood. Defects in cilial function are now documented in several other human diseases including autosomal recessive polycystic kidney disease, nephronophthisis, Bardet-Biedl syndrome and many animal models of polycystic kidney disease. Therapeutic trials in these animal models of polycystic kidney disease have identified several promising drugs that ameliorate disease severity. However, elucidation of the function of the polycystins and the primary cilium will have a major impact on our understanding of renal cystic diseases and will create exciting new opportunities for the design of disease-specific therapies.

Animals↗
PubMed2006

Cystatin C and prognosis for cardiovascular and kidney outcomes in elderly persons without chronic kidney disease.

BACKGROUND: Cystatin C is an alternative measure of kidney function that may have prognostic importance among elderly persons who do not meet standard criteria for chronic kidney disease (estimated glomerular filtration rate [GFR] > or =60 mL/min per 1.73 m2). OBJECTIVE: To evaluate cystatin C as a prognostic biomarker for death, cardiovascular disease, and incident chronic kidney disease among elderly persons without chronic kidney disease. DESIGN: Cohort study. SETTING: The Cardiovascular Health Study, a population-based cohort recruited from 4 communities in the United States. PARTICIPANTS: 4663 elderly persons. MEASUREMENTS: Measures of kidney function were creatinine-based estimated GFR by using the Modification of Diet in Renal Disease equation and cystatin C concentration. Outcomes were death, cardiovascular death, noncardiovascular death, heart failure, stroke, myocardial infarction, and incident chronic kidney disease during follow-up (median, 9.3 years). RESULTS: At baseline, 78% of participants did not have chronic kidney disease (estimated GFR > or =60 mL/min per 1.73 m2) and mean cystatin C concentration, creatinine concentration, and estimated GFR were 1.0 mg/L, 79.6 micromol/L (0.9 mg/dL), and 83 mL/min per 1.73 m2, respectively. Cystatin C concentrations (per SD, 0.18 mg/L) had strong associations with death (hazard ratio, 1.33 [95% CI, 1.25 to 1.40]), cardiovascular death (hazard ratio, 1.42 [CI, 1.30 to 1.54]), noncardiovascular death (hazard ratio, 1.26 [CI, 1.17 to 1.36]), incident heart failure (hazard ratio, 1.28 [CI, 1.17 to 1.40]), stroke (hazard ratio, 1.22 [CI, 1.08 to 1.38]), and myocardial infarction (hazard ratio, 1.20 [CI, 1.06 to 1.36]) among these participants. Serum creatinine concentrations had much weaker associations with each outcome and only predicted cardiovascular death. Participants without chronic kidney disease who had elevated cystatin C concentrations (> or =1.0 mg/L) had a 4-fold risk for progressing to chronic kidney disease after 4 years of follow-up compared with those with cystatin C concentrations less than 1.0 mg/L. LIMITATIONS: Because this study did not directly measure GFR or albuminuria, the extent to which cystatin C may be influenced by nonrenal factors was not determined and participants with albuminuria might have been misclassified as having no kidney disease. CONCLUSIONS: Among elderly persons without chronic kidney disease, cystatin C is a prognostic biomarker of risk for death, cardiovascular disease, and chronic kidney disease. In this setting, cystatin C seems to identify a "preclinical" state of kidney dysfunction that is not detected with serum creatinine or estimated GFR.

Aged↗
PubMed2005

Interfaces between cardiovascular and kidney disease among Aboriginal Australians.

Rates of kidney disease among several indigenous groups have been shown to be substantially higher than corresponding non-indigenous groups. This excess has been clearly shown among Aboriginal Australians with respect to both end-stage kidney disease and early kidney disease. Rates of cardiovascular disease among Aboriginal Australians are also very high, as are rates of diabetes, smoking, and possibly overweight and obesity. These factors have been traditionally linked with cardiovascular and renal disease as part of a broader "metabolic syndrome." However, the links and interfaces between cardiovascular and kidney disease in this environment extend beyond these "traditional" factors. The factors associated with atherosclerosis have expanded in recent years to include markers of inflammation, some infection, antioxidants, and other "non-traditional" risk factors. Given the high rates of acute infection and poor living conditions endured by many indigenous people, one might expect these "non-traditional" risk factors to be highly prevalent. In this review, we explore the relationships between markers of inflammation, some serological markers of infection, and other selected markers and both cardiovascular and renal disease. In doing so, we demonstrate links between kidney and cardiovascular disease at a number of levels, beyond the "traditional" cardiovascular/renal risk factors. Many of these factors are beyond the control of the individual or even community; addressing these issues a broader focus and biopsychosocial model.

Australia↗
PubMed1995

Gender-dependent disease severity in autosomal polycystic kidney disease of rats.

The impact of gender on the course of chronic renal failure in polycystic kidney disease (PKD) has been under discussion for years. Recently an animal model of autosomal dominant PKD in the rat became available allowing this topic to be studied. The aim of this study was to evaluate disease severity according to gender, and the occurrence of anticipation and/or genetic imprinting. Male and female affected PKD rats were crossed with respective Wistar-Ottawa-Karlsburg (WOK) rats. From this P generation 26 affected F1 hybrids were obtained, which were then backcrossed with WOK rats, resulting in 275 backcrosses (BC generation). In BC rats the affected males had a significantly higher kidney weight, worse histology and poorer renal function than the females. In the male, but not the female rats of the BC generation, transmission from an affected F1 mother resulted in significantly higher kidney weight, worse histology and poorer renal function than when the gene was inherited through an affected father. Since at the same time body and kidney weight were higher in the respective unaffected males, the previous effect in the affected rats might be due to a growth factor transferred by the mother's milk. The sex of the P generation had no such impact on these parameters. Thus our data provide no evidence for disease anticipation and genetic imprinting (in the classical sense) in the PKD rats, and the assumption of a gender-dependent disease expressivity is favored.

Animals↗
PubMed2002

The genes and proteins associated with poly-cystic kidney diseases.

Genetically based polycystic kidney diseases include autosomal dominant (ADPKD) and recessive (ARPKD) polycystic kidney diseases, nephronophthisis and medullary cystic disease. The PKD1 and PKD2 genes responsible for ADPKD and their respective encoded proteins polycystin-1 and polycystin-2 are under intense study and clues are developing as to their function and roles in the disease process. Structure-function analysis suggests that polycystins form multiprotein complexes with focal adhesion and cell-cell adherens junction proteins, which then initiate intracellular signaling events culminating in regulation of transcription of genes controlling proliferation and differentiation. Although less is known about the PKHD-encoded fibrocystin responsible for ARPKD or about the NPH1-encoded nephrocystin responsible for nephronophthisis, it is proposed that they function in the same cellular pathway involving protein-protein interactions, signal transduction and regulation of gene transcription. ADPKD epithelia are more adherent to collagen, less migratory, fail to recruit FAK to polycystin complexes and show aberrant, persistent expression of the fetal genes Erb-B2 and beta2 subunit of NaK-ATPase after birth. It is suggested that the function of the polycystin complex is to act as a key developmental regulator of renal tubule morphogenesis.

DNA Mutational Analysis↗
PubMedDate not supplied

Variable renal disease progression in autosomal dominant polycystic kidney disease: a role for nitric oxide?

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by a variable renal disease progression, which is primarily due to genetic heterogeneity (PKD1 vs. PKD2). Evidence obtained in murine models and studies of variability in siblings and twins suggest that modifier genes influence renal disease progression in ADPKD. These modifier loci could affect cystogenesis and/or cyst progression, but also more general factors, i.e. endothelial dysfunction. The demonstration of endothelial dysfunction in Pkd1(+/-) mice and ADPKD patients, and the effect of the frequent Glu298Asp polymorphism of ENOS on renal disease progression in ADPKD suggest that an impaired release of nitric oxide (NO) by endothelial cells can accelerate renal function degradation. These results also suggest that polycystins can participate in the regulation of endothelial NO synthase (eNOS) and that addressing endothelial dysfunction in ADPKD can offer a new perspective to slow renal disease progression.

Animals↗
PubMedDate not supplied

Glomerulocystic kidney disease: MRI findings.

Glomerulocystic kidney disease (GCKD) is a rare form of renal cystic disease characterized by cystic dilation of Bowman's capsule. The imaging findings of small renal cysts with a predominant cortical and subcapsular distribution allows for distinction from other, more common, polycystic kidney diseases. The appearance and distribution of the renal cysts by magnetic resonance imaging allow for a definitive diagnosis of GCKD.

Aged↗
PubMed2006

Molecular and cellular pathogenesis of autosomal recessive polycystic kidney disease.

Autosomal recessive polycystic kidney disease (ARPKD) is an inherited disease characterized by a malformation complex which includes cystically dilated tubules in the kidneys and ductal plate malformation in the liver. The disorder is observed primarily in infancy and childhood, being responsible for significant pediatric morbidity and mortality. All typical forms of ARPKD are caused by mutations in a single gene, PKHD1 (polycystic kidney and hepatic disease 1). This gene has a minimum of 86 exons, assembled into multiple differentially spliced transcripts and has its highest level of expression in kidney, pancreas and liver. Mutational analyses revealed that all patients with both mutations associated with truncation of the longest open reading frame-encoded protein displayed the severe phenotype. This product, polyductin, is a 4,074-amino acid protein expressed in the cytoplasm, plasma membrane and primary apical cilia, a structure that has been implicated in the pathogenesis of different polycystic kidney diseases. In fact, cholangiocytes isolated from an ARPKD rat model develop shorter and dysmorphic cilia, suggesting polyductin to be important for normal ciliary morphology. Polyductin seems also to participate in tubule morphogenesis and cell mitotic orientation along the tubular axis. The recent advances in the understanding of in vitro and animal models of polycystic kidney diseases have shed light on the molecular and cellular mechanisms of cyst formation and progression, allowing the initiation of therapeutic strategy designing and promising perspectives for ARPKD patients. It is notable that vasopressin V2 receptor antagonists can inhibit/halt the renal cystic disease progression in an orthologous rat model of human ARPKD.

Animals↗
PubMed2003

Drug-induced kidney diseases.

Drug-induced kidney disease constitutes an important cause of acute renal failure and chronic kidney disease in present day clinical practice. Different classes of drugs, by virtue of immunological mechanisms or direct toxicity initiate certain stereotyped renal responses. For most patients suffering from drug-induced nephropathy common risk factors which precipitate the adverse effects include: old age, volume -depleted state, pre-existing renal dysfunction and coexisting use of other nephrotoxins. Although it is impossible to present all the drugs causing renal disease, a few prototype drugs are mentioned. In a case of undiagnosed renal disease a possibility of drug-induced renal failure should be kept as the prompt removal of the drug and supportive management can reverse the renal dysfunction to a large extent.

Humans↗
PubMed1996

Anticipation of end-stage renal disease in autosomal dominant polycystic kidney disease.

Recently, anticipation of renal failure, i.e. earlier onset of end-stage renal disease in successive generations, has been reported in autosomal dominant polycystic kidney disease. In order to evaluate differences in length of time in reaching end-stage renal disease, we examined 55 families with accurate information about renal death. In 12 families the average difference between the age at renal death in 17 parent-offspring pairs was 7.7 years (range from -5 to 22 years). This value was significantly greater than zero (P = 0.0004). Thus, a substantial decrease in the age at renal death in the offspring as compared with the parent has been observed in this group of families.

Age of Onset↗