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PubMed2005

Surgical indications and procedures of parathyroidectomy in patients with chronic kidney disease.

The Kidney Foundation of the USA proposed clinical practice guidelines for bone metabolism and disease in chronic kidney disease including parathyroidectomy (PTx). We performed PTx in a total of 1725 patients with advanced secondary hyperparathyroidism (2HPT) and evaluated the K/DOQI guideline concerning PTx, comparing it with our surgical strategy. The guidelines emphasize the avoidance of ectopic calcification and cardiovascular complications which may be induced by hypercalcemia, hyperphosphatemia, and persistent high parathyroid hormone level. We agree with the attitude of the K/DOQI guideline. To decide surgical indications, we emphasize that the size of parathyroid gland is one of the important factors. The guideline recommends subtotal PTx and total PTx with autotransplantation. We prefer total PTx with forearm autograft, mainly because it is easier and safer to remove the residual parathyroid tissue from the forearm at recurrence compared to neck re-exploration. In Japan, almost all patients require long-term hemodialysis after PTx because of the very small opportunity of kidney transplantation. The risk of recurrence is not negligible. Based on our huge experience we believe our strategy for advanced secondary hyperparathyroidism can be accepted at least in Japan.

Calcium↗
PubMed2005

Elevated blood pressure and risk of end-stage renal disease in subjects without baseline kidney disease.

BACKGROUND: Many cases of end-stage renal disease (ESRD) are ascribed to hypertension. However, because renal disease itself can raise blood pressure, some investigators argue that ESRD seen in patients with hypertension is due to underlying primary renal disease. Previous cohort studies of the relationship between blood pressure and ESRD did not uniformly screen out baseline kidney disease. METHODS: We conducted a historical cohort study among members of Kaiser Permanente of Northern California, a large integrated health care delivery system. The ESRD cases were ascertained by matching with the US Renal Data System registry. RESULTS: A total of 316 675 adult Kaiser members participated in the Multiphasic Health Checkups from 1964 to 1985. All subjects had estimated glomerular filtration rates of 60 mL /min per 1.73 m(2) or higher and negative dipstick urinalysis results for proteinuria or hematuria. During 8 210 431 person-years of follow-up, 1149 cases of ESRD occurred. Compared with subjects with a blood pressure less than 120/80 mm Hg, the adjusted relative risks for developing ESRD were 1.62 (95% confidence interval [CI], 1.27-2.07) for blood pressures of 120 to 129/80 to 84 mm Hg, 1.98 (95% CI, 1.55-2.52) for blood pressures of 130 to 139/85 to 89 mm Hg, 2.59 (95% CI, 2.07-3.25) for blood pressures of 140 to 159/90 to 99 mm Hg, 3.86 (95% CI, 3.00-4.96) for blood pressures of 160 to 179/100 to 109 mm Hg, 3.88 (95% CI, 2.82-5.34) for blood pressures of 180 to 209/110 to 119 mm Hg, and 4.25 (95% CI, 2.63-6.86) for blood pressures of 210/120 mm Hg or higher. Similar associations between blood pressure level and ESRD risk were seen in all subgroup analyses. CONCLUSIONS: Even relatively modest elevation in blood pressure is an independent risk factor for ESRD. The observed relationship does not appear to be due to confounding by clinically evident baseline kidney disease.

Adult↗
PubMedDate not supplied

[Polycystic liver disease without autosomal dominant polycystic kidney disease].

Polycystic liver disease is characterized by the presence of multiple bile duct-derived epithelial cysts scattered in the liver parenchyma. The natural history and clinical manifestations of polycystic liver disease are based on the disease as it manifests in patients with autosomal dominant polycystic kidney disease (ADPKD). The occurrence of polycystic liver disease independently from polycystic kidney disease has been known for a long time. More recently, a gene for autosomal dominant polycystic liver disease has been identified on chromosome 19p 13.2-13.1. Isolated polycystic liver disease is underdiagnosed and genetically distinct from polycystic liver disease associated with ADPKD but with similar pathogenesis and clinical manifestations. We report here two men with polycystic liver disease no associated with ADPKD. Ultrasound and computed tomography imaging were effective in documenting the underlying lesions non-invasively.

Adult↗
PubMed1996

Hepatic cystic disease in an adult polycystic kidney disease transplant population.

BACKGROUND: A study of the incidence of polycystic liver in a transplant population and an assessment of the impact of this disease on the group was undertaken. Clinical presentation, investigation and treatment of hepatic polycystic disease are explored. METHODS: The study examined the morbidity incurred by polycystic liver disease in patients, patient and graft survival, incidence of hepatic cysts and presentation, investigation and management of morbid hepatic cystic disease. One hundred and eleven patients were studied. RESULTS: It was found that hepatic cysts occurred in the majority of patients that underwent transplants for renal failure because of polycystic kidney disease at this institution. Symptomatic hepatic cystic disease was found to be primarily responsible for three deaths and affected between 15 and 20% of the group. Gall bladder disease was found to be associated with highly symptomatic hepatic cystic disease. CONCLUSION: Hepatic cystic disease is common in patients that have had kidney transplants because of polycystic kidney disease. Morbidity is likely to increase as patients survive for longer periods. Cholecystectomy should be considered in patients with significant hepatic cystic disease.

Adult↗
PubMed2006

Development of polycystic kidney disease in juvenile cystic kidney mice: insights into pathogenesis, ciliary abnormalities, and common features with human disease.

Significant progress in understanding the molecular mechanisms of polycystic kidney disease (PKD) has been made in recent years. Translating this understanding into effective therapeutics will require testing in animal models that closely resemble human PKD by multiple parameters. Similar to autosomal dominant PKD, juvenile cystic kidney (jck) mice develop cysts in multiple nephron segments, including cortical collecting ducts, distal tubules, and loop of Henle. The jck mice display gender dimorphism in kidney disease progression with more aggressive disease in male mice. Gonadectomy experiments show that testosterone aggravates the severity of the disease in jck male mice, while female gonadal hormones have protective effects. EGF receptor is overexpressed and mislocalized in jck cystic epithelia, a hallmark of human disease. Increased cAMP levels in jck kidneys and activation of the B-Raf/extracellular signal-regulated kinase pathway are demonstrated. The effect of jck mutation on the expression of Nek8, a NIMA-related (never in mitosis A) kinase, and polycystins in jck cilia is shown for the first time. Nek8 overexpression and loss of ciliary localization in jck epithelia are accompanied by enhanced expression of polycystins along the cilia. The primary cilia in jck kidneys are significantly more lengthened than the cilia in wild-type mice, suggesting a role for Nek8 in controlling ciliary length. Collectively, these data demonstrate that the jck mice should be useful for testing potential therapies and for studying the molecular mechanisms that link ciliary structure/function and cystogenesis.

Animals↗
PubMed1992

Factors affecting the progression of renal disease in autosomal-dominant polycystic kidney disease.

Autosomal-dominant polycystic kidney disease results in renal failure at a varying age from childhood to old age. We postulated that factors other than the culprit gene alone contribute to the course of progression of the renal failure. We studied 580 subjects with autosomal-dominant polycystic kidney disease and 194 unaffected family members. We calculated survival curves to end-stage renal failure or death and developed a linear model for testing the effects of single or multiple variables on the progression of renal failure as estimated from the reciprocal of serum creatinine. Fifty-two subjects died and 94 reached end-stage renal failure during the period of observation, yielding functional survivals of 71% at age 50 years, 53% at 58 years and 23% at 70 years. The following variables were independently associated with worse mean renal function at a given age (P value less than 0.01): the PKD1 gene, younger age at diagnosis, male gender, hypertension, increased left ventricular mass, hepatic cysts in women, three or more pregnancies, gross hematuria, urinary tract infections in men and renal size expressed as renal volume. The following were not associated significantly with the course of renal function: gender of affected parent, mitral valve prolapse, intracranial aneurysms, any pregnancy, hepatic cysts in men and urinary tract infections in women. The identification of unalterable maleficent factors such as the PKD1 gene and male gender permit more informed counseling while the identification of alterable factors such as hypertension, number of pregnancies and recurrent urinary tract infections provides the clinician with the opportunity to modify these factors and improve the management of patients with autosomal-dominant polycystic kidney disease.

Adult↗
PubMed2005

Clinical practice guidelines in nephrology: evaluation, classification, and stratification of chronic kidney disease.

The National Kidney Foundation developed and oversees the Kidney Disease Outcomes Quality Initiative, a process that develops clinical practice guidelines in nephrology. Recent guidelines address the evaluation, classification, and stratification of chronic kidney disease (CKD). These guidelines provide, for the first time, a standard definition of CKD, classification of its stages, and suggestions for appropriate laboratory measurements for the assessment of kidney function. Also discussed are the association of level of kidney function with systemic complications that develop during CKD, and the risk of loss of kidney function and development of cardiovascular disease in CKD.

Chronic Disease↗
PubMed2006

New therapeutic option for autosomal dominant polycystic kidney disease patients with enlarged kidney and liver.

The kidneys of patients with autosomal dominant polycystic kidney disease (ADPKD) usually continue to increase in size even after patients begin dialysis, and mass effects can lead to severe complications. Thus far, renal manifestations of this disorder have been discussed only from the viewpoint of cyst formation or cytogenesis, not from that of vascular abnormality. Because kidneys in ADPKD patients are usually supplied by well-developed arteries, we attempted renal contraction therapy in ADPKD patients with renal transcatheter arterial embolization (TAE) using intravascular coils. Mainly peripheral branches of renal arteries encircling the cysts were embolized. Our treatment has been confirmed to be effective in 266 patients until 2005. Renal size continued to decrease to 53% of the pre-TAE after 1 year. Almost all patients have had improved quality of life and nutritional status. We next tried TAE in 76 intractable patients with symptomatic polycystic liver. We tried to embolize only the hepatic segments replaced by cystic lesions in which the hepatic arteries were well-developed but the intrahepatic portal vein was obstructed. Sixty-four patients have had a good clinical course with this method. Based on our observation of ADPKD through treatment with TAE, we speculate that cyst growth in both the kidney and the liver progresses via the mechanism of 'arteriogenesis' of large vessels as well as 'angiogenesis' of small vessels.

Cysts↗
PubMed2005

Biomarkers of inflammation and progression of chronic kidney disease.

BACKGROUND: Chronic kidney disease is associated with higher levels of inflammatory biomarkers. Statins have anti-inflammatory properties and may attenuate loss of kidney function. Although inflammation may mediate progressive renal injury, the relation between statin use, markers of inflammation, and the rate of kidney function loss has not been elucidated. We examined the association between pravastatin use, levels of C-reactive protein (CRP), soluble tumor necrosis factor receptor II (sTNFrii), and the rate of kidney function loss. METHODS: We performed a post hoc analysis of data from a randomized placebo controlled trial of pravastatin 40 mg daily in people with previous myocardial infarction. Glomerular filtration rate (GFR) was estimated using the Modification of Diet in Renal Disease Study (MDRD) GFR equation. We studied 687 subjects with chronic kidney disease (GFR < 60 mL/min/1.73 m(2)) who did not experience a cardiovascular event during follow-up. Multivariate linear regression was used to study the relation between baseline CRP and sTNFrii and the rate of kidney function loss in mL/min/1.73 m(2)/year. Cross-product interaction terms were used to determine if these relations varied with pravastatin use. RESULTS: Median baseline GFR was 54.5 mL/min/1.73 m(2) (interquartile range 49.7, 57.8) and median duration of follow-up was 58 months. Higher baseline CRP level was independently associated with more rapid kidney function loss (highest tertile 0.6 mL/min/1.73 m(2) per year faster than lowest tertile) (P= 0.001). A similar independent relation was observed between tertile of sTNFrii and rate of kidney function loss (highest tertile 0.5 mL/min/1.73 m(2) per year faster than lowest tertile) (P= 0.006). Subjects with both CRP and sTNFrii in the highest tertile ("inflamed" status) appeared to derive more renal benefit from pravastatin than those without (P for interaction 0.047). In these 108 subjects, renal function loss in pravastatin recipients was 0.8 mL/min/1.73 m(2)/year slower than placebo (95% CI 0 to 1.5 mL/min/1.73 m(2)/year slower) (P= 0.039). CONCLUSION: Higher CRP and sTNFrii are independently associated with faster rates of kidney function loss in chronic kidney disease. Pravastatin appears to prevent loss of kidney function to a greater extent in individuals with greater evidence of inflammation, although this was of borderline significance. These data suggest that inflammation may mediate the loss of kidney function among subjects with chronic kidney disease and concomitant coronary disease.

Adult↗
PubMed2006

Cardiovascular disease risk factors in chronic kidney disease: overall burden and rates of treatment and control.

BACKGROUND: Mild to moderate chronic kidney disease (CKD) is associated with increased risk for cardiovascular disease. The burden of cardiovascular disease risk factors in this setting is not well described. METHODS: We compared the age- and sex-adjusted prevalence of cardiovascular disease risk factors and their treatment and control among persons with and without CKD in 3258 Framingham offspring cohort members who attended the seventh examination cycle (1998-2001). Glomerular filtration rate (GFR) was estimated using the simplified Modification of Diet in Renal Disease Study equation. We defined CKD as a GFR of less than 59 mL/min per 1.73 m(2) in women and less than 64 mL/min per 1.73 m(2) in men. RESULTS: Those with CKD were older, more likely to be obese (33.5% vs 29.3%; P=.02), and more likely to have low levels of high-density lipoprotein cholesterol (45.2% vs 29.4%; P<.001) and high triglyceride levels (39.9% vs 29.8%; P<.001). Those with CKD had a higher prevalence of hypertension (71.2% vs 42.7%; P<.001) and hypertension treatment (86.0% vs 72.5%; P<.001), but were less likely to achieve optimal blood pressure control (27.0% vs 45.5%; P<.001). Participants with CKD had a higher prevalence of elevated low-density lipoprotein cholesterol levels (60.5% vs 44.7%; P=.06) and lipid-lowering therapy (57.1% vs 42.6%; P=.09), although this was not statistically significant. A greater proportion of individuals with CKD than those without had diabetes (23.5% vs 11.9%; P=.02) and were receiving diabetes treatment (63.6% vs 46.9%; P=.05), but were less likely to achieve a hemoglobin A(1c) level of less than 7% (43.8% vs 59.4%; P=.03). CONCLUSIONS: Chronic kidney disease is associated with a significant burden of cardiovascular disease risk factors in the community. The diagnosis of CKD should alert the practitioner to look for potentially modifiable cardiovascular risk factors.

Aged↗
PubMed1987

Third trimester ultrasonic presentation of infantile polycystic kidney disease.

Infantile polycystic kidney disease (Potter's Type 1) is an autosomal recessive disorder that affects the kidneys and liver. Use of ultrasound to make the diagnosis prenatally is well documented and, in fact, it is advocated as a screening device for second-trimester identification of potentially affected fetuses. The sonographic appearance is characterized by enlarged hyperechoic kidneys, enlarging fetal abdominal circumference, and oligohydramnios. It is suggested that a ratio of the kidney circumference to the abdominal circumference (KC/AC) be used as method of quantifying renal size and as a potential indicator of early kidney enlargement associated with infantile polycystic kidney disease (IPKD). We report a case of serial ultrasound examination of a pregnancy at risk for IPKD where the in utero diagnosis was not established until the third trimester.

Adult↗
PubMed1986

Antenatal diagnosis of renal anomalies with ultrasound. IV. Bilateral multicystic kidney disease.

Bilateral multicystic kidney disease is a congenital disorder that is fatal in the newborn period. A series of nine cases of bilateral multicystic kidney disease diagnosed prenatally by ultrasound is presented. Ultrasound criteria necessary for the diagnosis are bilateral multicystic kidneys, loss of renal architecture, nonvisualization of the fetal bladder, and absence of amniotic fluid. Seven of the nine cases had autopsy confirmation of the diagnosis. Three cases had other associated congenital anomalies. Precise prenatal diagnosis may allow patients the option of elective abortion or may prevent unnecessary obstetric intervention. We propose that a reliable diagnosis can be made with prenatal ultrasound.

Female↗
PubMed2005

AGE-RAGE and AGE Cross-link interaction: important players in the pathogenesis of diabetic kidney disease.

At present, diabetic kidney disease affects about 15 - 25% of all type 1 diabetic patients and 20 - 40% of all patients with type 2 diabetes. The mechanisms underlying the development of diabetic kidney disease are extremely complex and not yet fully understood. Among the many potential pathogenic mechanisms responsible for the progression in diabetic kidney disease, the involvement of metabolic factors beyond blood glucose (such as advanced glycation end products (AGEs)) has been suggested. This review will present the emerging evidence in support of a significant role of AGE formation in the development of diabetic kidney disease. AGEs mediate their effects through two main pathways - through a receptor-independent AGE cross-link formation pathway and through a receptor-dependent pathway where AGEs bind to specific cell surface associated receptors, the receptor for AGE (RAGE) being the most well-characterised so far. First, we will describe the AGE-RAGE system, including its localisation in the normal kidney, and then move on to discuss in vitro and in vivo studies (that is, experimental and clinical data) in support of a pathogenic role of AGE-RAGE and AGE cross-link interaction in the development of diabetic kidney disease. Finally, the effects of known and potential inhibitors of AGE-RAGE and AGE cross-link systems in diabetic kidney disease will be examined.

Animals↗