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PubMed2000

[Active uremia therapy in autosomal dominant polycystic kidney disease].

BACKGROUND: Autosomal dominant polycystic kidney disease is the most frequent inheritable kidney disease. Epidemiological studies have not been performed in Norway. MATERIAL AND METHODS: Based on the Norwegian Renal Registry, we retrospectively studied 375 patients diagnosed with this disease taken into renal replacement therapy between 1980 and 1997. They were compared with patients with glomerulonephritis. RESULTS: The average age for autosomal dominant polycystic kidney disease patients at start of renal replacement therapy was 55.2 years with a significant difference (p < 0.003) between men (53.7 years) and women (57.1 years). 295 patients (78.7%) were transplanted while 80 (21.3%) were not transplanted. From start of renal replacement therapy autosomal dominant polycystic kidney disease patients had a significantly higher (p = 0.0002) five year survival rate (70%) compared with glomerulonephritis patients (60%). One and five year patient survival rates were significantly higher (p = 0.0006) for living donor recipients (95% and 90%) compared with necro-kidney recipients (90% and 75%). One year graft survival rates for kidneys from living donors was 90% and 80% for necro-kidneys, after five years the graft survival rate was 80% and 65% (p = 0.0026). After an average of five years, 227 (60.5%) patients are alive, 197 with functioning kidney grafts (87%) while 30 (13%) are on dialysis. INTERPRETATION: Male autosomal dominant polycystic kidney disease patients start renal replacement therapy earlier than female patients. Autosomal dominant polycystic kidney disease patients do have better patient survival in renal replacement therapy than patients with glomerulonephritis.

Adult↗
PubMed1998

Lack of function of an N-ethylmaleimide-sensitive thiol protein in erythrocyte membrane of autosomal dominant polycystic kidney disease.

The polycystic kidney disease 1 (PKD1) gene product polycystin has been predicted to be an integral membrane protein involved in cell-cell and cell-matrix interactions. The erythrocyte membrane fluidity in autosomal dominant polycystic kidney disease (ADPKD) patients is increased, and this may be due to a membrane cytoskeletal abnormality. The abnormal erythrocyte sodium-lithium countertransport kinetics in-ADPKD are related to an altered thiol protein in the cytoskeleton. The possibility that a similar thiol protein abnormality causes the increased erythrocyte membrane fluidity in ADPKD was investigated. The membrane fluidity of intact erythrocytes from 12 ADPKD patients and 12 healthy control subjects was assessed from the fluorescence anisotropies of 1,6-diphenyl-1,3,5-hexatriene (DPH) and trimethylammonium-diphenyl-hexatriene (TMA-DPH). The effect on membrane fluidity of N-ethylmaleimide (NEM), cytochalasin D, heating at 48 degrees C for 20 min, or more specifically, liposomes containing antibodies to actin or ankyrin, was determined. In erythrocytes from healthy control subjects, the fluorescence anisotropy of DPH (mean +/- SEM: 0.223 +/- 0.001) was decreased after treatment with NEM (0.200 +/- 0.003, P < 0.001), cytochalasin D (0.206 +/- 0.006, P < 0.001), heating (0.199 +/- 0.002, P < 0.001), and antibodies to actin (0.194 +/- 0.002, P < 0.001) or ankyrin (0.196 +/- 0.002, P < 0.001). The TMA-DPH anisotropy (0.279 +/- 0.001) was also decreased after treatment with NEM (0.264 +/- 0.001, P < 0.001), cytochalasin D (0.264 +/- 0.001, P < 0.001), heating (0.265 +/- 0.001, P < 0.001), and antibodies to actin (0.262 +/- 0.002, P < 0.001) or ankyrin (0.262 +/- 0.002, P < 0.001). NEM had no additional effect on the other treatments, suggesting that its target thiol protein was associated with the cytoskeleton. In untreated erythrocytes from ADPKD patients, fluorescence anisotropies of both DPH and TMA-DPH were reduced, and none of the treatments altered the anisotropy of either DPH or TMA-DPH. In ADPKD, a cytoskeletal thiol protein is abnormal and possibly explains abnormal lipid bilayer properties and transport protein function in erythrocytes in this disease.

Actins↗
PubMedDate not supplied

[Cystic kidney disease].

The kidney is one of the organs most frequently affected by cystic disease, which can be defined as the morbidity attributable to the presence of renal cysts. Renal cysts appear in a series of very diverse hereditary anomalies, acquired or developmental, occurring as an isolated form or in association with other renal or systemic alterations. Cysts are microscopic or macroscopic abnormal cavities, with saccular or fusiform shape, coated with epithelium and filled with liquid. They origin in the nephron or the collecting tubules, with which a connection can be maintained or not. They can occur at any point in life, from the prenatal period to adulthood, and one or both kidneys may be affected in a focal or diffuse form. Renal cyst pathogenesis is not completely understood, although there is evidence that it may be caused by hyperproliferative dysplasic secretion and matrix remodelling alterations, modulated by endocrine, paracrine, juxtacrine and autocrine stimuli, which induce obstructive alterations that are determinant in its genesis and evolution.

Adult↗
PubMed2003

Epidemiology of cardiovascular risk in patients with chronic kidney disease.

BACKGROUND: Chronic kidney disease (CKD) patients are highly prone to cardiovascular disease for a number of reasons. At the time of starting renal replacement treatment, their cardiovascular condition is already severely compromised, suggesting that cardiovascular risk factors begin to operate very early in the progression of CKD. Moreover, those patients reaching end-stage renal disease without cardiovascular abnormalities have a high probability of developing de novo cardiovascular disease. METHODS: In this review, we analyse the prevalence of the major cardiovascular risk factors in CKD patients and their importance as contributors to the excess cardiovascular disease in this population. We also describe and discuss the main results obtained in the management of these risk factors in terms of preventing cardiovascular morbidity and mortality. RESULTS: Hypertension plays a major role in determining cardiac damage at all stages of CKD, including the dialytic phase. Anaemia is a major determinant of the development of left ventricular hypertrophy and therefore its correction can be expected to improve cardiovascular status and long-term survival, but this needs to be done before changes in cardiac structure become well established. Calcium-phosphate disorders are increasingly acknowledged to be cardiovascular risk factors in CKD, yet their medical control is still far from being satisfactory. Dyslipidaemia is particularly frequent in CKD patients, but the benefit of lipid-lowering treatments still has to be proven. Finally, CKD is associated with newly recognized risk factors for atherosclerosis, although their importance as cardiovascular risk factors is still controversial. CONCLUSIONS: Nephrologists should attempt to give optimal treatment for well-established cardiovascular risk factors, even if this generally fails to prevent the excess cardiovascular disease of CKD patients. Increasing attention is now being paid to newly recognized CKD-related risk factors for atherosclerosis, although their real importance is still under debate and, before therapeutic prescriptions can be applied to CKD patients, further studies in these new fields are needed.

Cardiovascular Diseases↗
PubMed1993

Glomerulocystic kidney disease--nosological considerations.

Glomerulocystic kidneys can be categorized into three major groups: (1) glomerulocystic kidney disease, comprising nonsyndromal heritable and sporadic forms of severely cystic kidneys in children and adults, (2) glomerulocystic kidneys in heritable malformation syndromes, and (3) glomerular cysts in dysplastic kidneys. The first category includes diffusely glomerulocystic kidneys in newborns and young children, many of whom have family histories positive for classical polycystic kidney disease. No differences between familial and sporadic cases have been identified, apart from the family histories. The sporadic cases are conceivably new mutations of the same disease. The first category also includes sporadic and familial disease in older children and adults. The inheritance in adult familial disease, as in childhood familial disease, has been dominant. An apparently distinct entity is hypoplastic glomerulocystic kidney disease, a dominant reported in only a few families. These kidneys, apart from being glomerulocystic, are small, and imaging studies show abnormal pyelocaliceal anatomy. The second category includes glomerulocystic kidneys as major components of heritable syndromes such as tuberous sclerosis, orofaciodigital syndrome, brachymesomelia-renal syndrome, trisomy 13, and the short rib-polydactyly syndromes. The category also includes glomerular cysts in several syndromes, namely Jeune syndrome and familial juvenile nephronophthisis, better known for chronic progressive tubulointerstitial disease. Glomerular cysts occur as a minor component, i.e., scattered cortical cysts, in several other syndromes, among them Zellweger's, in which the cysts are typically present and are usually inconsequential, only occasionally serious enough to affect renal function. In all of these syndromes, the cysts are inconsistently expressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2026

Effects of Progressive Inspiratory Muscle Training on Lung Volume and Respiratory Strength in Patients With Pre-Dialysis Chronic Kidney Disease.

INTRODUCTION: Chronic kidney disease can present changes in thoracic cavity volume and respiratory muscle weakness, even in the pre-dialysis stage. However, there is little evidence on the effects of inspiratory muscle training in these patients. METHODS: This was a randomized clinical trial which comprised patients with Chronic Kidney Disease in stages 3, 4, and 5 undergoing conservative treatment, allocated experimental group (EG) with progressive loading (up to 50% of maximal inspiratory pressure [MIP]) and control group (CG) with a fixed load (5 cmH2O) and no load progression performed daily for 8&#xa0;weeks. The outcomes assessed were thoracic cavity volumes, as measured by optoelectronic plethysmography, and inspiratory and expiratory respiratory muscle strength. RESULTS: A total of 30 patients completed the study. All volumes significantly increased at the end of the protocol with a large effect size, but only the pulmonary thoracic cavity volume showed a significant interaction (F&#xa0;=&#xa0;3.698; p&#xa0;=&#xa0;0.042). There was an increase in inspiratory muscle strength in the EG (73.88-90.35&#xa0;cmH2O; p&#xa0;<&#xa0;0.001) and in the CG (70.85-86.92&#xa0;cmH2O; p&#xa0;=&#xa0;0.001), as well as in expiratory muscle strength in the EG (97.71-108.53&#xa0;cmH2O; p&#xa0;=&#xa0;0.001) and in the CG (80.69-94.77&#xa0;cmH2O; p&#xa0;=&#xa0;0.004). CONCLUSION: Daily IMT increased thoracoabdominal volumes, particularly pulmonary rib cage volume in the progressive-load group, as well as respiratory muscle strength in patients with pre-dialysis CKD. However, progressive-load IMT was not superior to minimal-load training.

Humans↗
PubMed2005

Effects of anemia and left ventricular hypertrophy on cardiovascular disease in patients with chronic kidney disease.

Left ventricular hypertrophy (LVH) and anemia are highly prevalent in moderate chronic kidney disease (CKD). Because anemia may potentiate the adverse effects of LVH on cardiovascular outcomes, the effect of both anemia and LVH on outcomes in CKD was examined. Data from four community-based longitudinal studies were pooled: Atherosclerosis Risk in Communities Study, Cardiovascular Health Study, Framingham Heart Study, and Framingham Offspring Study. Serum creatinine levels were calibrated indirectly across studies, and GFR was estimated using the Modification of Diet in Renal Disease equation. CKD was defined as GFR between 15 and 60 ml/min per 1.73 m(2). LVH was based on electrocardiogram criteria. Anemia was defined as hematocrit <36% in women and 39% in men. The primary outcome was a composite of myocardial infarction, stroke, and death; a secondary cardiac outcome included only myocardial infarction and fatal coronary heart disease. Among 2423 patients with CKD, 96% had electrocardiogram and anemia data. Median follow-up was 102 mo. In adjusted analysis, LVH was associated with increased risk for composite and cardiac outcomes (hazard ratio [HR], 1.67 [95% confidence interval (CI), 1.34 to 2.07] and 1.62 [95% CI, 1.18 to 2.24], respectively), whereas anemia was associated with increased risk for the only composite outcome (HR, 1.51 [95% CI, 1.27 to 1.81]). The combination of anemia and LVH was associated with an increased risk for both study outcomes compared with individuals with neither risk factor (HR, 4.15 [95% CI, 2.62 to 6.56] and 3.92 [95% CI, 2.05 to 7.48]; P = 0.02 and 0.01 for interaction term, respectively). The combination of anemia and LVH in CKD identifies a high-risk population.

Aged↗
PubMed1992

Autosomal recessive polycystic kidney disease.

Autosomal recessive polycystic kidney disease is a rare inherited disorder which usually becomes clinically manifest in early childhood, whereas autosomal dominant polycystic kidney disease usually is a disorder of adult onset. With increasing knowledge and improving diagnostic techniques, it becomes evident that the spectrum of both entities is much more variable than generally known. The presentation of autosomal recessive polycystic kidney disease at later ages and survival into adulthood have been reported. The diagnostic criteria, clinical course, genetics and differential diagnosis of autosomal recessive polycystic kidney disease will be presented.

Caroli Disease↗
PubMed2003

Disease progression and outcomes in chronic kidney disease and renal transplantation.

BACKGROUND: It is unknown whether renal transplant recipients (RTR) have better outcomes and disease progression rates compared to patients with chronic kidney disease (CKD) when matched for the level of kidney function. METHODS: We analyzed data on 1762 patients with CKD (N = 872) and RTR (N = 890) over 16 years, applying the new Kidney/Disease Outcomes Quality Initiative (K/DOQI) staging system for CKD in a single center retrospective study. Patients were further divided based their native kidney disease. We determined disease progression by the slope of creatinine clearance decline and patient and kidney survival rates adjusted for age, gender and stage of kidney function, using Cox proportional hazards models. RESULTS: The overall rate of creatinine clearance decline in patients with CKD was -6.6 +/- 8.7 mL/min/year compared to -1.9 +/- 4.7 mL/min/year in RTR (P < 0.0001). The rate of decline per stage of CKD was also significantly lower in RTR. Whereas overall kidney survival was higher in RTR compared to patients with CKD (49.6% vs. 17.2%, respectively, P < 0.001), patient survival was not statistically different between the two groups (74.7% vs. 80.3%, respectively, P = 0.25). CONCLUSION: RTR had similar mortality rates compared to patients with CKD despite enjoying slower rates of disease progression and better kidney survival rates. These data suggest that RTR are a unique subset of patients with CKD whose comorbid conditions likely offset the potential benefits of slower rates of progression.

Adult↗
PubMed2005

Subclinical peripheral arterial disease in patients with chronic kidney disease: prevalence and related risk factors.

BACKGROUND: Atherosclerotic artery disease is a common condition in patients with chronic kidney disease (CKD); however, there are few published data on the prevalence of peripheral arterial disease (PAD) in nondialyzed patients with renal insufficiency. The ankle-brachial index (ABI) is a simple, noninvasive, and reliable method to assess PAD. METHODS AND RESULTS: Prevalence of PAD using ABI was investigated in 102 patients referred for the first time to a nephrology clinic with CKD in stages 3 to 5 of the K/DOQI classification, and with no previous diagnosis of PAD. Patients with ABI <0.9 were considered positive for PAD. A total of 64% of the patients were male. The mean age was 70 +/- 11 (range 58-84) years, and the estimated creatinine clearance (CrCl) was 35 +/- 12 (range 6-59) mL/min(-1). Of the total sample, 26% were diabetics, 10% active smokers, 48% ex-smokers, and 29% had a diagnosis of coronary heart disease (CHD), 15% had been previously diagnosed of stroke, and 17% had signs and symptoms compatible with intermittent claudication, which had passed unnoticed. Thirty-two percent of patients had an ABI <0.9 (mean 0.64 +/- 0.25). Of these patients with PAD, 84% were men (P < 0.005), and only 30% presented a clinical picture compatible with intermittent claudication. Absolute risk of CHD according to the Framingham 1998 score was higher in the PAD group (19.3% +/- 6 vs. 13.1% +/- 8; P= 0.01). Patients with PAD were older (75 +/- 6 vs. 66 +/- 11 years, P= 0.000), and had worse renal function (CrCl 30.8 +/- 12 vs. 37 +/- 10.7 mL.min(-1), P= 0.016) compared to patients without PAD, but no differences were found in cholesterol levels (total, HDL, LDL), calcium, phosphorus, or PTH. In the logistic regression analysis, independent indicators of PAD risk were male sex, age, and lower CrCl. Twelve percent of patients had an ABI > or =1.3, suggestive of parietal arterial calcifications. In these patients, systolic blood pressure and pulse pressure were lower (126 +/- 18 vs. 150 +/- 27, P= 0.005, and 52 +/- 13 vs. 68 +/- 25 mm Hg, P= 0.044), i-PTH levels were higher (228 +/- 267 vs. 117 +/- 63 pg/mL, P= 0.01), and a larger proportion of this group was treated with calcitriol (34% vs. 13%) compared to patients with a normal ABI. CONCLUSION: A high prevalence of PAD, considered as an ABI <0.9, was demonstrated in nondialyzed patients with CKD. This was related with age, male sex, and higher degree of renal insufficiency, while the presence of ABI > or =1.3 was associated with a greater degree of hyperparathyroidism. These data show the need to carry out routine ABI determinations in patients with CKD for early detection of peripheral arterial disease.

Aged↗
PubMed2001

Survival after end-stage renal disease in autosomal dominant polycystic kidney disease: contribution of extrarenal complications to mortality.

Autosomal dominant polycystic kidney disease (ADPKD) accounts for 8% to 10% of patients with end-stage renal disease (ESRD) in the United States and Europe. Progressive expansion of multiple bilateral renal cysts leads to massive enlargement of the kidneys and progressive renal failure. Extrarenal manifestations of ADPKD, such as liver cysts, intracranial aneurysms, cardiac valvular disease, and perhaps diverticulosis, have been documented extensively in cross-sectional studies, but little is known about their natural history. It is thought that extrarenal aspects of ADPKD contribute to increased mortality, yet survival on dialysis of the ADPKD population surpasses that of the general dialysis population. To address this issue, we analyzed the relative risk and causes of death after ESRD in ADPKD versus nondiabetic controls using data from the United States Renal Data System. Relative risk of death from any cause, including the major extrarenal manifestations of ADPKD, was determined as a function of ESRD treatment modality (dialysis or transplantation). We found a lower total mortality rate in ADPKD ESRD patients compared with nondiabetic control ESRD patients (relative risk of death in ADPKD = 0.57; P < 0.001). Mortality rates of extrarenal complications except for polycystic liver disease were similar or lower in ADPKD patients than in nondiabetic controls. Mortality secondary to extrarenal complications was substantially lower than that secondary to cardiovascular or cerebrovascular disease.

Adult↗
PubMed2000

Laparoscopic nephrectomy in patients with end-stage renal disease and autosomal dominant polycystic kidney disease.

Autosomal dominant polycystic kidney disease (ADPKD) is often characterized by end-stage renal disease (ESRD) and problems including pain, hematuria, and infection. Open nephrectomy is curative; however, the morbidity of the procedure is considerable. Between 1995 and 1998, 11 laparoscopic nephrectomies were performed on nine symptomatic patients (five men and four women) with ESRD and ADPKD. Two patients underwent a staged bilateral laparoscopic nephrectomy. All patients presented with abdominal or flank pain and an abdominal mass. Other clinical problems included hypertension in eight patients, urinary tract infections in two patients, and gross hematuria in one patient. Seven patients were receiving long-term dialysis treatment, and two patients had undergone prior renal transplantation. Patients were evaluated for preoperative and postoperative pain, analgesic use, hospital course, and convalescence. The overall average operative time was 6.3 hours, with an average estimated blood loss of 153 mL. Eight nephrectomy specimens were removed by morcellation, and three specimens were removed intact through a 7- to 12-cm incision. The average hospital stay was 3 days, and the average time to normal activity was 5 weeks. With a mean follow-up of 31 months, all nine patients reported elimination of their preoperative pain based on a pain analogue score. Six major and two minor complications occurred, including blood transfusion, a vena cavotomy, splenic cyanosis, pulmonary embolism, clotted arteriovenous fistula, and brachial plexus injury. Incisional hernias occurred in two of the three patients who underwent open removal. One patient noted improvement, and two patients noted resolution of their hypertension postoperatively. Laparoscopic nephrectomy in patients with ADPKD and ESRD offers an effective alternative to open nephrectomy to manage renal-related pain. This procedure provides the benefits of minimal intraoperative blood loss, minimal postoperative pain, brief hospital stay, and rapid convalescence.

Aged↗
PubMed1995

[Skin changes in kidney diseases and in chronic kidney insufficiency].

Skin symptoms in renal disease occur in a series of rare inherited or acquired diseases affecting the kidneys as well as the skin (amyloidosis, vasculitis, angiokeratoma diffusum corporis Fabry) (table 1). Chronic renal failure, regardless of its origin, often causes important skin symptoms, such as pruritus, the typical complexion with elastosis seen in uremic patients, porphyria cutanea uremica, metastatic calcifications, skin necrosis due to uremic small arteries disease with medial calcification and intimal hyperplasia, perforating dermatoses, nail lesions and symptoms of the oral mucosa (table 2). The following article reviews the pathogenesis and the limited possibilities of treatment for skin symptoms in chronic renal failure.

Folliculitis↗
PubMed2006

Sleeping disorders in patients with end-stage renal disease and chronic kidney disease.

About 85% of patients on maintenance hemodialysis have sleep disorders that depend on comorbidities, age, morning dialytic shift, and blood pressure. They are ameliorated by erythropoietin, by transplantation, and by daily and nocturnal dialysis. Some data exist on sleep disorders in CKD patients, and show that lack of a refreshing sleep is present even at early stages of the disease and may affect 82.2% of patients without any relationship to comorbidities.

Circadian Rhythm↗
PubMed2005

Barriers to successful care for chronic kidney disease.

BACKGROUND: The National Kidney Foundation has formulated clinical practice guidelines for patients with chronic kidney disease (K/DOQI). However, little is know about how many patients actually achieve these goals in a dedicated clinic for chronic kidney disease. METHODS: We performed a cross-sectional analysis of 198 patients with an estimated glomerular filtration rate of less than 30 ml/min/1.73 m2 and determined whether K/DOQI goals were met for calcium, phosphate, calcium-phosphate product, parathyroid hormone, albumin, bicarbonate, hemoglobin, lipids, and blood pressure. RESULTS: We found that only a small number of patients achieved K/DOQI targets. Recent referral to the nephrologist, failure to attend scheduled clinic appointments, African American ethnicity, diabetes, and advanced renal failure were significant predictors of low achievement of K/DOQI goals. CONCLUSION: We conclude that raising awareness of chronic kidney disease and K/DOQI goals among primary care providers, early referral to a nephrologist, the exploration of socioeconomic barriers and cultural differences, and both patient and physician education are critical to improve CKD care in patients with Stage 4 and 5 CKD.

Black or African American↗
PubMedDate not supplied

Management of heart failure and coronary artery disease in patients with chronic kidney disease.

Cardiovascular disease (CVD) is a major contributor to the mortality and morbidity of patients who suffer from chronic kidney disease (CKD). Heart failure and ischemic heart disease (IHD) are both highly prevalent in this population. The diagnosis of myocardial dysfunction is usually based on echocardiography. As in the general population, systolic dysfunction is treated with a combination of diuretics, renin-angiotensin system blockade, and beta-receptor antagonists. Diastolic dysfunction is best managed by eliminating the cause. Non-invasive tests for coronary artery disease (CAD) may be less reliable in patients with renal disease compared with nonuremic patients. Medical therapy of IHD in this population is generally similar to that for other patient groups, but surgical revascularization appears to carry a higher risk of complications with poorer clinical outcomes. The choice of revascularization procedure (coronary artery bypass grafting versus percutaneous transluminal angioplasty) should be based on the specific coronary anatomy of a given patient as well as a consideration of other comorbid factors.

Angioplasty, Balloon, Coronary↗