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At least 217 records · Page 12Linked to original sources
PubMed1995

Apoptosis and loss of renal tissue in polycystic kidney diseases.

BACKGROUND: Polycystic kidney disease is characterized by the enlargement of renal cysts, interstitial fibrosis, and gradual loss of normal renal tissue in association with progressive deterioration of renal function. The process causing the progressive loss of renal tissue is unknown, but it could be the result of a form of programmed cell death known as apoptosis. METHODS: We assayed apoptotic DNA fragmentation in normal and polycystic kidneys biochemically by gel electrophoresis and histochemically by in situ end-labeling. A DNA-specific dye, Hoechst 33258, was used to detect morphologic apoptosis in renal samples from patients with normal kidneys, polycystic kidney disease, and other kidney diseases. RESULTS: Apoptotic DNA fragmentation was detected in polycystic kidneys from 5 patients without renal failure and 11 patients with renal failure but not in kidneys from 12 patients with no renal disease. In situ end-labeling revealed apoptotic cells in glomeruli, in cyst walls, and in both cystic and noncystic tubules of the polycystic kidneys. No tubular apoptosis was detected in renal-biopsy specimens from five patients with IgA nephropathy, three patients with nephrosclerosis, two patients with focal glomerulosclerosis, one patient with diabetic nephropathy, six patients with acute tubular necrosis, or four patients with acute and four patients with chronic renal-transplant rejection. The capacity of polycystic kidney cells to undergo apoptosis was retained in vitro in the absence of uremia, ischemia, and other confounding pathologic conditions. CONCLUSIONS: Apoptotic loss of renal tissue may be associated with the progressive deterioration of renal function that occurs in patients with polycystic kidney disease.

Animals↗
PubMed2005

Coronary artery disease and peripheral vascular disease in chronic kidney disease: an epidemiological perspective.

The enormous burden of CAD and PVD inpatients who have CKD contributes substantially to increased morbidity and mortality. The increased risk of vascular disease observed in CKD patients is likely to be multifactorial, with contributions from traditional and nontraditional cardiovascular factors. Given the overwhelming evidence on the known benefits of cardioprotective medications, their underuse remains puzzling in a population at enormous risk. During the past 5 years, the research community and national interest groups have made significant progress in organizing a concerted approach to improve the management of patients who have CKD and vascular disease. Much work remains to be done. The development of national guidelines in the management of these patients at high risk for future cardiovascular events will be a welcome step. The evaluation of multitargeted interventions for reduction of cardiovascular risk through randomized clinical trials is desperately needed. Finally, the low use of known cardioprotective strategies in this high-risk group is a serious issue and warrants immediate attention at local and national levels.

Chronic Disease↗
PubMed1991

Acquired renal cystic disease mimicking adult polycystic kidney disease in a patient undergoing long-term hemodialysis.

Acquired renal cystic disease (ARCD) is defined as the development of multiple cysts in the renal cortex and medulla in patients with chronic renal failure who are free from congenital polycystic kidney disease. ARCD develops generally in contracted kidneys. We report a case of grotesque enlargement of a single kidney in a patient who had been receiving hemodialysis for 18 years. Although the exact causes of ARCD are not known, 3 factors may contribute to the development of nephromegaly; the sex, the duration of hemodialysis and previous unilateral nephrectomy. As in polycystic disease, when the involved kidney reaches considerable size, ARCD may have a favorable effect on anemia caused by chronic renal failure.

Adult↗
PubMed2006

Implications of chronic kidney disease for dietary treatment in cardiovascular disease.

Chronic kidney disease (CKD) often accompanies cardiovascular disease (CVD). Trends foretelling a greater burden of CKD and CVD are largely a result of increasing frequencies of obesity, hypertension, and diabetes. Nutritional therapy occupies a critical role in reducing risk factors and preventing progressive damage to the kidneys and heart. Nutritional assessment and treatment should take into account both health concerns. This review examines several diet components and eating styles for efficacy in the treatment of these conditions. A variety of dietary regimens claim to provide health benefits, but rigorous scientific validation of long-term efficacy is frequently lacking. An urgent need exists for eating styles that reduce risk of chronic diseases and that are acceptable and achievable in free-living populations. We describe our ongoing study, a randomized controlled trial comparing the American Heart Association Step II diet and a Mediterranean diet, in survivors of a first myocardial infarction. The primary end point is a composite of mortality and major CVD events. Because many in this population have CKD, indicators of kidney damage and function are prespecified secondary end points. Results of this trial should provide insight into optimal dietary interventions for persons with both CVD and CKD.

Cardiovascular Diseases↗
PubMed2000

Effects of potassium citrate/citric acid intake in a mouse model of polycystic kidney disease.

The kidney function in a model of autosomal dominant polycystic kidney disease (PKD), the Han:SPRD rat, is dramatically improved by chronic ingestion of a solution of potassium citrate and citric acid (KCitr). This study investigated whether this treatment would also be beneficial in the pcy/pcy mouse, a model of autosomal recessive PKD. Starting at 1 month of age, male CD-1 pcy/pcy and normal CD-1 mice were provided with a solution of 55 mM K(3) citrate/67 mM citric acid or tap water to drink. The pcy/pcy mice on the KCitr solution failed to grow normally and showed elevated plasma urea levels when compared to water-drinking littermates. Growth of normal CD-1 mice was not affected by KCitr intake. The pcy/pcy mice were then provided with a more dilute solution of KCitr to drink: this resulted in greater kidney wet and dry weights and a higher kidney weight/body weight ratio, but no beneficial effects. We conclude that pcy/pcy mice cannot tolerate a high level of KCitr intake and that a lower level is of no benefit. Whether KCitr therapy would be helpful in patients with PKD is still an open question.

Animals↗
PubMed2004

Chronic kidney disease progression in native and transplant kidneys.

PURPOSE OF REVIEW: The present review addresses the recent literature demonstrating important differences in the rate of progression of kidney function decline between transplant recipients and patients with native kidney disease. It also highlights the need for prospective studies to determine the importance of nonimmune factors that are established risk factors for progression of native kidney disease in the transplant setting. RECENT FINDINGS: Transplant recipients establish modest levels of kidney function but have rates of kidney function decline that are slower than those in patients with native kidney disease. Continued improvements in long-term graft survival have not been achieved despite significant advances in immunosuppression. There is increasing observational evidence that nonimmune factors that play a causal role in progression of native kidney disease may also be important determinants of allograft decline. There are fundamental differences between transplant recipients and patients with native kidney disease that preclude extrapolation of evidence from native kidney disease to the transplant setting. SUMMARY: Transplant recipients are a unique group of chronic kidney disease patients. Prospective studies to determine the importance of nonimmune factors such as hypertension, proteinuria, dyslipidemia, diabetes, and anemia in the transplant setting are needed.

Disease Progression↗
PubMedDate not supplied

[Left ventricular hypertrophy in chronic kidney disease].

Chronic kidney disease (CKD) is associated with increased cardiovascular (CV) risk. Left ventricular (LV) hypertrophy (LVH), together with coronary artery disease, has been considered the main target of intervention. LVH is highly prevalent in CKD even in early stages, as compared to general non-selected population. This is mainly due to the multifactorial pathogenesis of LVH in renal patients where both haemodynamic and non-haemodynamic stimuli synergically act inducing either an increase in left ventricular mass or an LV dilation. Anaemia and arterial hypertension seem to be the most important factors. Interventional studies have shown that partial correction of anaemia through epoetin, together with an arterial hypertension successful therapy through renin-angiotensin system acting drugs, such as ACE-inhibitors, were able to induce a LVH regression in CKD. Indeed, the unfavourable outcome in patients with both CKD and LVH, whose survival is reduced and incidence of fatal and non-fatal CV events increased, can be reversed if LVH is regressed by therapy. The most promising strategy in CKD seems to be LVH early diagnosis through echocardiography, the correct screening of risk factors, a LVM longitudinal monitoring through echo, as well as starting treatment in the early stages of CKD, with the aim of improving general and CV prognosis for these patients.

Anemia↗
PubMed2005

Etiology and management of hypertension in chronic kidney disease.

The kidneys are vital in the pathogenesis of hypertension and are also pathologically affected by the presence of hypertension. The prevalence of hypertension in chronic kidney disease (CKD) depends on age, the severity of renal failure, and proteinuria. The intricate and inextricable relationship between CKD and hypertension seems to cause cardiovascular disease that has assumed epidemic proportions. This article discusses the etiology and treatment of hypertension in CKD so that it can be better controlled.

Humans↗
PubMed1993

Aneurysms of coronary arteries in a patient with adult polycystic kidney disease: arteriosclerosis or involvement by the primary disease?

Adult polycystic kidney disease is frequently associated with gastrointestinal and cardiovascular abnormalities. These include hypertension, mitral valve prolapse, mild dilation of the aortic root, abdominal aneurysms, and predisposition to aortic, mitral, and tricuspidal valve regurgitation reminiscent of Marfan's syndrome. Although the exact molecular mechanisms of adult polycystic kidney disease are not well established, a generalized defect of collagen structure is hypothesized. The most severe vascular problems, however, are typical intracranial aneurysms with a high incidence of subarachnoid hemorrhage and a high mortality rate. We report a case of dilated coronary arteries found incidentally in a patient with adult polycystic kidney disease and stress-induced angina pectoris. The typical angina pectoris of the patient is explained by left ventricular hypertrophy and coronary heart disease. Multiple liver cysts, mitral valve prolapse, and the coronary aneurysms in this patient with adult polycystic kidney disease appear to reflect the manifestation of a generalized connective tissue disorder in this syndrome.

Adult↗
PubMed1984

The diagnosis of congenital renal anomalies with ultrasound. II. Infantile polycystic kidney disease.

Infantile polycystic kidney disease in an autosomal recessive disorder which in its severe form is characterized by bilateral renal enlargement and renal failure. The present study was undertaken to assess the diagnostic accuracy of antenatal sonography in a population at risk. Nineteen patients with fetuses at risk for infantile polycystic kidney disease were referred for ultrasound examination to the Perinatal Unit at Yale-New Haven Hospital. Ten infants had infantile polycystic kidney disease (53%). A positive antenatal sonographic diagnosis was made by the presence of oligohydramnios, an absent urinary bladder, bilateral renal enlargement as measured by the kidney circumference-to-abdominal circumference ratio, and the typical hyperechogenic appearance of the kidneys in the disease. A correct antenatal diagnosis was made in nine of the 10 affected infants. There were no false positive diagnoses. A false negative diagnosis occurred in an infant with a less severe form of the disease. Ultrasound is a valuable tool in the antenatal diagnosis of infantile polycystic kidney disease.

False Negative Reactions↗
PubMed2000

Genetic evidence for a trans-heterozygous model for cystogenesis in autosomal dominant polycystic kidney disease.

Polycystic kidney disease (ADPKD) is a condition with an autosomal dominant mode of inheritance and adult onset. Two forms of the disease, ADPKD1 and ADPKD2, caused by mutations in PKD1 and PKD2, respectively, are very similar, except that ADPKD1 patients run a more severe course. At the cellular level, ADPKD1 was first shown to be recessive, since somatic second hits are perhaps necessary for cyst formation. The near identical phenotype had suggested that ADPKD1 and ADPKD2 might have a similar pathogenesis and that the two gene products, poly- cystins 1 and 2, are part of a common developmental pathway. Work in transgenic mice showed that somatic loss of Pkd2 expression is necessary for renal cyst formation, and recently we showed that somatic mutations inactivating the inherited healthy allele were present in 9 of 23 cysts from a human ADPKD2 kidney, supporting a two-hit loss-of-function model for ADPKD2 cystogenesis. Here, we provide the first direct genetic evidence that polycystins 1 and 2 do interact, perhaps as part of a larger complex. In cystic DNA from a kidney of an ADPKD1 patient, we showed somatic mutations not only in the PKD1 gene of certain cysts, but also in the PKD2 gene of others, generating a trans -heterozygous state with mutations in both genes. One mutation in PKD1 is of germinal nature and the mutation in the PKD2 gene is of somatic nature. The implications of such a situation are enormous, not only for ADPKD, but also for many other conditions with phenotypic heterogeneity and age-dependent penetrance.

Amino Acid Sequence↗
PubMed1989

Caroli's disease and adult polycystic kidney disease: a rarely recognized association.

Caroli's disease is a rare form of fibropolycystic disease of the hepatobiliary system characterized by segmental cystic dilatation of intrahepatic ducts. It is associated with intrahepatic cholelithiasis, cholangitis and hepatic abscesses. Like other forms of fibropolycystic disease of the liver, Caroli's disease is often accompanied by cystic renal disease, specifically renal tubular ectasia or medullary sponge kidney. Adult-type polycystic kidney disease associated with Caroli's disease is rare, only one such case having appeared in the literature to our knowledge. We present a second instance of this association.

Bile Duct Diseases↗
PubMed1998

Role and long-term results of laparoscopic decortication in solitary cystic and autosomal dominant polycystic kidney disease.

PURPOSE: Access to retroperitoneal structures via the laparoscope has become established for various conditions. This minimally invasive approach has distinct advantages over conventional open surgery. We document our experience with laparoscopic cyst decortication for diseases of the kidney, including simple and complex cysts, multiple cysts and autosomal dominant polycystic kidney disease. MATERIALS AND METHODS: We retrospectively reviewed the records of 17 patients who underwent a total of 20 procedures. Cases were categorized as polycystic kidney disease and nonpolycystic kidney disease. Factors analyzed were estimated blood loss, length of surgical procedure, hospital stay and complications. Followup included radiographic studies (computerized tomography and/or renal sonography) and patient subjective pain relief, as determined by clinical records and telephone interview. RESULTS: Nine and 11 procedures were done for nonpolycystic kidney disease and polycystic kidney disease, respectively. Of the 8 patients with polycystic kidney disease 3 underwent repeat procedures. Followup was 3 to 63 months (average 26). All patients with simple cysts who were treated for pain were pain-free at the latest followup. Of the 10 procedures 9 (90%) performed for pain relief in polycystic kidney disease successfully produced immediate pain relief. Pain-free status decreased with time with 7 of 8 (87.5%) pain-free after 6 months, and 5 of 7 (71.4%) at 1, 4 of 6 (66.7%) at 2 and 1 of 4 (25%) at 3 years. A repeat operation successfully relieved recurrent pain in 2 of 3 cases (66.7%). Of the 7 patients with polycystic kidney disease who underwent surgery for pain relief 5 (71%) are currently pain-free. CONCLUSIONS: Laparoscopic renal cyst decortication is an effective minimally invasive treatment for painful simple cysts. It is also effective for short to intermediate pain relief in autosomal dominant polycystic kidney disease. Long-term followup suggests that a repeat procedure may be necessary to maintain adequate control of symptoms in polycystic kidney disease.

Adult↗
PubMed2003

The role of renin-angiotensin-aldosterone system inhibition in chronic kidney disease.

Chronic kidney disease (CKD) is emerging as a new health pandemic. Underlying the global rise in CKD is an increase in diabetes, hypertension and other cardiovascular risk factors leading to progressive renal dysfunction. Emerging evidence strongly suggests that achieving target blood pressure goals via inhibition of the renin-angiotensin-aldosterone system confers significant renal and cardioprotection for patients with CKD. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) lower blood pressure, reduce proteinuria and reduce both the progression of CKD and adverse cardiovascular events. The role of aldosterone inhibition and combination therapy, such as ACEI/ARB, in CKD are under investigation. As our understanding of the basic mechanisms underlying CKD progression advances, novel therapies targeting post-translational endothelial and mesangial messengers downstream from angiotensin II and aldosterone may become available for clinical use.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

The exclusion of patients with chronic kidney disease from clinical trials in coronary artery disease.

Chronic kidney disease (CKD) is associated with a high risk of death from coronary artery disease and may modify the response to standard cardiovascular therapies. Treatment of subjects with CKD should ideally be based on evidence from randomized, clinical trials, but how often subjects with CKD have been excluded from these trials is uncertain. We undertook this study in order to quantify how often subjects with moderate to advanced CKD were excluded from large cardiovascular trials. MEDLINE and the reference list of selected articles were searched in order to identify large, randomized, controlled trials of five different coronary artery disease therapies published between 1998 and 2005. Exclusion criteria and reported clinical characteristics of subjects were abstracted. Rates of exclusion and reporting of baseline characteristics of study participants were compared for CKD, diabetes, history of smoking, and hypertension. Eighty-six trials randomizing 411 653 patients were identified. More than 80% of trials excluded subjects with end-stage renal disease and 75.0% excluded patients with CKD. Subjects with diabetes, hypertension, or a history of smoking were excluded less than 4% of the time. Baseline renal function of study participant was reported in only 7% of trials. Patients with CKD are frequently excluded from coronary artery disease trials and renal function of randomized subjects is rarely reported. These findings reinforce the notion that available data on the treatment of coronary artery disease in subjects with CKD have significant limitations and should be generalized to the treatment of subjects with CKD cautiously.

Adrenergic beta-Antagonists↗