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PubMed2005

Emerging therapies for polycystic kidney disease.

Polycystic kidney diseases are the most common, monogenetic, inherited diseases in humans. Numerous human genes or gene loci are associated with a renal cystic phenotype. Currently, there are no treatments available to slow the development of renal cystic pathology; however, animal studies have identified several potential approaches to intervene in the disease process. The most advanced therapy is the use of vasopressin V(2) receptor antagonists, which reduce renal cAMP, a known promoter of renal cystic enlargement. Other therapies under study include the use of c-myc antisense oligonucleotides and epidermal growth factor receptor tyrosine kinase inhibitors. Considering the diverse genes that cause renal cysts and the multiorgan involvement of these diseases, multiple therapeutic approaches will eventually be necessary to treat these diseases.

Animals↗
PubMed2006

The case for disease management in chronic kidney disease.

Chronic kidney disease (CKD) is a growing epidemic in the United States and worldwide, with nearly two thirds of CKD patients also having diabetes, hypertension, or both. Morbidity and mortality among patients with CKD are high, as are the costs associated with care, which is highly fragmented. Disease management (DM) programs are designed to coordinate the delivery of care to patients, improve clinical outcomes, and reduce costs along the continuum of care. The goals of DM programs in CKD patients are to fill the gaps in current care by focusing on four key areas: (1) slowing the progression of CKD, (2) identifying and managing the complications of CKD, (3) identifying and managing associated comorbid conditions, and (4) smoothing the transition to renal replacement therapy (RRT). To be successful, this approach requires multidisciplinary collaboration among physicians (eg, primary care physicians, endocrinologists, cardiologists, nephrologists, surgeons) and participating caregivers including nurses, dieticians, social workers, and pharmacists. Patient identification, limited reimbursement, late patient referral, and lack of primary care physician and nephrologist knowledge about the importance and details of CKD management are all barriers that must be overcome for such programs to be successfully implemented. Considering the magnitude of the opportunity, DM applied to CKD is a promising approach to the care of this vulnerable population.

Comorbidity↗
PubMed2004

Cardiovascular risk in chronic kidney disease.

National Kidney Foundation guidelines define chronic kidney disease (CKD) as persistent kidney damage (confirmed by renal biopsy or markers of kidney damage) and/or glomerular filtration rate (GFR) <60 mL/min/1.73m2 for greater than three months. Patients with CKD experience higher mortality and adverse cardiovascular (CV) event rates, which remains significant after adjustment for conventional coronary risk factors. This progressive CV risk associated with worsening renal function may be explained by other factors that become increasingly important with renal decline. In this regard, more investigation of nonconventional factors that have received a lot of attention includes associations with inflammation, albuminuria, reduced vascular compliance, and homocysteine. In addition, individuals with CKD encounter the problem of "therapeutic nihilism," in which there is a lack of appropriate risk factor modification and intervention, despite established awareness of their high cardiovascular risk. Several studies suggest that these individuals derive as much, if not more, benefit from evidence-based cardiovascular therapies and strategies. Greater educational efforts are needed to reduce this therapeutic gap.

Cardiovascular Diseases↗
PubMed2005

Sonographic assessment of the severity and progression of autosomal dominant polycystic kidney disease: the Consortium of Renal Imaging Studies in Polycystic Kidney Disease (CRISP).

BACKGROUND: The accuracy and precision of ultrasonography (US) in assessing the severity of autosomal dominant polycystic kidney disease (ADPKD) is unknown. METHODS: US and magnetic resonance imaging (MRI) were performed at baseline and 1 year on 230 subjects with ADPKD. Ellipsoid volume was calculated from US length, width, and depth, and sequential transverse images were used to measure total and cystic volume directly. These were compared with MRI measurements of kidney volume and cystic volume. RESULTS: Variability between different sonographers ranged from 18% to 42%. Correlations between US and MRI volume were 0.88 and 0.89. The SD of the discrepancy from MRI ranged from 21% to 33% and was unrelated to kidney size or body mass. Kidney length was the most reproducible measurement, and its correlation with MRI volume was 0.84. All patients with an US volume less than 700 cm3 had an MRI volume less than 1,000 cm3, and all patients with an US volume greater than 1,700 cm3 had an MRI volume greater than 1,000 cm3. Increases in volume after 1 year were 12% +/- 36% for the ellipsoid method, 6% +/- 29% for the direct method, and 4.2% +/- 7.2% for MRI. Correlation between US and MRI measurement of fractional cyst volume was 0.80. CONCLUSION: Sonographic measurement of kidney volume in patients with ADPKD is inaccurate and lacks the precision necessary to measure short-term disease progression. However, sonography can provide an estimate of kidney volume that reflects severity and prognosis in individual patients.

Adolescent↗
PubMed2005

Chinese herbal medicine in the treatment of chronic kidney disease.

Chronic kidney disease (CKD) is a worldwide public health issue with poor outcomes and high cost. There is growing evidence that some of the adverse outcomes of CKD can be prevented or delayed by early treatment using angiotensin II-converting enzyme inhibitors and angiotensin II-receptor blockers. A great amount of the world's population has been using traditional Chinese herbal medicine (TCHM) for treatment of CKD and has accumulated their experience for years. In this article, the knowledge and the therapeutic principles of traditional Chinese medicine in the treatment of CKD are briefly reviewed. The efficacy of several TCHMs, supported by either clinical evidence or experimental studies, is presented. The future direction for the study of Chinese herbal medicines in CKD is discussed.

Angelica↗
PubMed2003

Early detection of kidney disease in community settings: the Kidney Early Evaluation Program (KEEP).

BACKGROUND: Early identification of persons at risk for kidney disease provides an opportunity to prevent or delay its progression and decrease morbidity and mortality. Our hypothesis was that implementation of a targeted screening program in communities with high-risk populations would detect previously unidentified persons with or at high risk for chronic kidney disease (CKD) with a prevalence that exceeds that predicted for CKD in the general population. METHODS: Persons with hypertension or diabetes or a first-order relative with hypertension, diabetes, or kidney disease were screened for kidney disease risk factors. Blood pressure, blood glucose level, serum creatinine level, hemoglobin level, microalbuminuria, hematuria, pyuria, body mass index, and estimated glomerular filtration rate (EGFR) were evaluated. RESULTS: Six thousand seventy-one eligible persons were screened from August 2000 through December 2001: of these persons, 68% were women, 43% were African American, 36% were white, 10% were Hispanic, and 5% were Native American. Most reported high-school education or more (84%) and health insurance coverage (86%). Twenty-seven percent met the screening definitions for diabetes; 64%, for hypertension; 29%, for microalbuminuria; 8%, for anemia; 18%, for hematuria; 13%, for pyuria; 5%, for elevated serum creatinine level; 16%, for reduced EGFR; and 44%, for obesity. Among participants without a reported history of specified conditions, screening identified 82 participants (2%) with diabetes, 1,014 participants (35%) with hypertension, 277 participants (5%) with elevated serum creatinine levels, 839 participants (14%) with reduced EGFRs, and 1,712 participants (29%) with microalbuminuria. Thirty-five percent of participants with a history of diabetes had elevated serum glucose levels at screening (> or =180 mg/dL [10 mmol/L]), and 64% with a history of hypertension did not have blood pressure controlled to less than 140/90 mm Hg. Only 18% of participants with a history of diabetes and 31% with a reduced EGFR had blood pressure controlled to less than 130/80 mm Hg and less than 135/85 mm Hg, respectively. CONCLUSION: Targeted screening is effective in identifying persons with previously unidentified or poorly controlled kidney disease risk factors, as well as persons with a moderately decreased EGFR.

Adolescent↗
PubMed2006

Cardiometabolic syndrome and chronic kidney disease.

Chronic kidney disease (CKD) is increasingly recognized as a major risk factor for end-stage renal disease (ESRD), cardiovascular (CV) disease, and CV-related premature death. More than 8 million people in the United States have CKD; therefore, preventive stratiegies should be directed at identifying risk factors for this condition. There is growing evidence implicating the cardiometabolic syndrome, a clustering of CV risk factors that include obesity, insulin resistance, compensatory hyperinsulinemia, dysglycemia, atherogenic dyslipidemia, and hypertension. Factors mediating this relationship include increased glomerular filtration, increased vascular permeability, oxidative and endoplasmic reticulum stress, activation of the renin-angiotensin system, and inappropriate secretion of growth factors. The consequences are microalbuminuria, a marker of inflammation and endothelial dysfunction, renal vascular proliferation, extracellular matrix expansion, and CKD. Prevention of CKD should be directed at controlling all components of the cardiometabolic syndrome, with the ultimate goal of reducing the burden imposed by ESRD.

Albuminuria↗
PubMed1991

Sonographic, clinical and genetic aspects of prenatal diagnosis of cystic kidney disease.

Cystic kidneys or renal cystic disease is a morphologic description for an etiological heterogeneous group of disorders ranging from solitary cysts to several forms of multicystic and polycystic kidneys. The combination of the examination of the kidneys and liver, clinical data, family history and the presence of associated anomalies is mandatory to obtain a final diagnosis. The use of prenatal ultrasound to monitor pregnancies at risk for autosomal recessive polycystic kidney disease (ARPKD) is limited because a recurrence can be diagnosed early in pregnancy but may not be excluded. For pregnancies at risk for autosomal dominant polycystic kidney disease (ADPKD), a reliable prenatal diagnosis can only be provided by DNA studies after chorionic villus sampling. Cystic kidneys may present as part of different syndromes. An overview is given of the complex differential diagnosis. Dysplastic (multicystic) kidneys often occur unilaterally. In contrast with polycystic kidneys, diseased liver changes are not present in cystic dysplasia and prenatal ultrasound diagnosis is usually possible.

Chorionic Villi Sampling↗
PubMed2006

Arterial stiffness and enlargement in mild-to-moderate chronic kidney disease.

Chronic kidney disease (CKD) is associated with an increased risk of cardiovascular morbidity and mortality. Arterial stiffness and remodeling have been well documented in patients with end-stage renal disease, but little is known about arterial phenotype in CKD patients with moderate reduction in glomerular filtration rate (GFR). In total, 95 patients (58+/-15 years, mean+/-s.d.) with CKD and GFR measured by renal clearance of (51)Cr-ethylenediaminetetraacetate were compared to 121 hypertensive patients without CKD (59+/-11 years), and 57 normotensive subjects (56+/-6 years). Common carotid artery diameter, intima-media thickness (IMT), distensibility, and Young's elastic modulus were noninvasively determined with a high-definition echotracking system. Patients with CKD had a significantly larger carotid internal diameter than in hypertensives and normotensives (6.32+/-1.05, 5.84+/-0.74, and 5.50+/-0.64 m x 10(-3), respectively; P<0.001), resulting in 25% and 11% increases in circumferential wall stress, respectively, since no significant difference in IMT was observed. Carotid distensibility and elastic modulus did not significantly differ between CKD and hypertensives; normotensives had significantly higher distensibility and lower elastic modulus than CKD and hypertensive patients. Carotid-femoral pulse wave velocity was significantly higher in CKD patients than in hypertensives and normotensives. In multivariate analyses either involving the entire population or restricted to CKD patients, GFR was independently and strongly related to carotid diameter and elastic modulus. Arterial enlargement and increased arterial stiffness occur in parallel with the decline in renal function in patients with mild-to-moderate CKD.

Adult↗
PubMed2003

A controlled, prospective study of the effects of atorvastatin on proteinuria and progression of kidney disease.

BACKGROUND: Chronic kidney diseases, particularly if presenting with significant proteinuria, are commonly associated with substantial alteration of serum lipid levels. Experimental evidence suggests that lipid abnormalities may contribute to the progression of kidney disease. However, studies in humans on the subject are scarce. METHODS: In a prospective, controlled open-label study, the authors have evaluated the effects of one-year treatment with atorvastatin, a 3-hydroxy-3-methyglutaryl coenzyme A (HMG-CoA) reductase inhibitor, versus no treatment on proteinuria and progression of kidney disease in 56 patients with chronic kidney disease. Before randomization, all patients had already been treated for one year with angiotensin-converting enzyme (ACE) inhibitors or angiotensin AT1 receptor antagonists (ARBs) and other antihypertensive drugs. RESULTS: By the end of one-year treatment, urine protein excretion decreased from 2.2 +/- 0.1 to 1.2 +/- 1.0 g every 24 hours (P < 0.01) in patients treated with atorvastatin in addition to ACE inhibitor and ARBs. By contrast, urinary protein excretion decreased only from 2.0 +/- 0.1 to 1.8 +/- 0.1 g every 24 hours (P value not significant) in patients who did not receive atorvastatin in addition to ACE inhibitor or ARBs. During this time, creatinine clearance decreased only slightly and not significantly (from 51 +/- 1.8 to 49.8 +/- 1.7) in patients treated with atorvastatin. By contrast, during the same period of observation, creatinine clearance decreased from 50 +/- 1.9 to 44.2 +/- 1.6 mL/min (P < 0.01) in patients who did not receive atorvastatin. CONCLUSIONS: This study has shown that treatment with atorvastatin in addition to a regimen with ACE inhibitors or ARBs may reduce proteinuria and the rate of progression of kidney disease in patients with chronic kidney disease, proteinuria, and hypercholesterolemia. The benefits appear to occur in addition to those of treatment with ACE inhibitor and ARBs.

Anticholesteremic Agents↗
PubMed2005

Vitamin D and its analogues: do they protect against cardiovascular disease in patients with kidney disease?

BACKGROUND: Patients with chronic kidney disease (CKD) are at high risk for cardiovascular disease, and despite recent advances in hypertension control, anemia management, and dialysis adequacy, mortality remains high. Improved understanding of nontraditional risk factors, including those present at early phases in CKD, may lead to novel therapeutic strategies. CKD has been demonstrated to be an independent risk factor for cardiovascular disease in the general population, but data are lacking as to the associated potential abnormalities that occur in association with reduced glomerular filtration rate (GFR), which may contribute to this increased risk. Data are accumulating regarding the role of abnormalities of calcium, phosphorus, vitamin D, and parathyroid hormone (PTH) in cardiovascular disease. Vitamin D deficiency is present even in the early stages of CKD. Vitamin D plays a central role in calcium-phosphorus homeostasis, regulation of PTH, and formation and maintenance of bone. However, until recently, vitamin D has not been considered to have a biologic role in CKD beyond mineral regulation, or has been considered as a negative factor contributing to soft tissue and cardiovascular calcification. In light of recent observational studies showing an association of vitamin D therapy and survival benefit in hemodialysis patients, the effects of vitamin D on cardiovascular system have become a heavily debated issue. METHODS: A Medline search was performed to identify relevant literature describing the role of vitamin D in the pathogenesis of cardiovascular disease. Both the experimental and clinical literatures in English were reviewed. RESULTS: The accumulating published data demonstrate both associative relationships and mechanisms for biologic plausibility. The following three potential mechanisms may be important for the protective effects of vitamin D against cardiovascular disease mortality: vitamin D can inhibit various aspects of inflammation, which have been established as a key pathogenic mechanism in atherosclerosis; vitamin D exerts an antiproliferative effect on myocardial cell hypertrophy and proliferation, which underlies the pathogenesis of congestive heart failure; and vitamin D acts as a negative endocrine regulator for the renin-angiotensin system, which itself plays an important independent role in hypertension and cardiovascular health. CONCLUSION: Vitamin D deficiency might be an underestimated nonclassical risk factor for cardiovascular disease in CKD. Based on a review of the evidence, from both basic science and clinical studies, this article supports the possible protective role of vitamin D beyond its effect on mineral metabolism, and suggests the need for ongoing evaluation of the role of vitamin D in cardiovascular health in the CKD population.

Cardiovascular Diseases↗
PubMed1999

Isolated polycystic liver disease not linked to polycystic kidney disease 1 and 2.

Autosomal dominant polycystic liver disease occurs commonly in association with autosomal dominant polycystic kidney disease, types 1 and 2. It may also exist as a separate entity, genetically distinct from autosomal dominant polycystic kidney disease types 1 and 2, as has been recently established to exist in a Belgian family. We report here a large Argentinian family of Spanish-Belgian ancestry with autosomal dominant polycystic liver disease, where proximal and distal markers for both polycystic kidney disease 1 and 2 failed to demonstrate genetic linkage. The data support the notion that polycystic liver disease and autosomal dominant polycystic kidney disease may have separate chromosomal loci.

Adult↗
PubMedDate not supplied

Molecular genetics of polycystic kidney disease.

Polycystic kidney disease (PKD) is a major, multigene disorder that is characterized by the growth of large, fluid-filled cysts from the nephrons and collecting ducts of affected kidneys. At least three different genes are thought to give rise to the autosomal dominant (ADPKD) form of PKD. Two of the genes (PKD1 and PKD2) have now been isolated and sequenced, and based on their predicted structures are thought to encode proteins (polycystin-1 and polycystin-2) that function together as part of a multi-component membrane-spanning complex involved in cell-cell or cell-matrix interactions. Most mutations identified in affected families appear to be inactivating for the PKD1 and PKD2 genes, and recent evidence has suggested that a two-hit mechanism, in which the normal PKD1 allele is also inactivated, may be required for cyst growth. The large number of genes showing abnormal expression in cystic kidneys in humans and rodent models suggests that cellular processes associated with signal transduction, transcriptional regulation, and cell-cycle control are involved in cyst formation and that the cellular defect in PKD directly affects the regulation of epithelial differentiation.

Animals↗