Blood pressure control and kidney damage in hypertension: Results of a three-center cross-sectional study in North Central Nigeria.

BACKGROUND: Hypertension is one of the commonest cause of chronic kidney disease (CKD) in Nigerians. We describe blood pressure (BP) control and kidney disease markers in patients with hypertension as part of measures to curb the burden of this chronic debilitating disease. METHODS: Patients with hypertension in the main tertiary hospitals in three states in north central Nigeria were evaluated for indicators of CKD, including proteinuria and estimated glomerular filtration rate (eGFR) <60 ml/min/1.73 m2. Patients had their early morning first void urine tested for proteinuria using Combi-10 test strips. eGFR was estimated using the MDRD equation. RESULTS: A total of 1063 subjects (63.1% females and 36.8% males) with a mean age of 55 ± 11 years were studied. Diabetes mellitus (DM) was present in 214 (20.6%) and 422 (39.7%) had optimal BP control. The median duration of hypertension was 6 years (range 1-44 years). Proteinuria occurred in 130 (12.2%), while 212 (19.9%) had reduced eGFR and 46 (4.3%) had proteinuria and reduced eGFR. The use of calcium channel blockers [adjusted odds ratio (AOR): 0.70, 95% Confidence Interval (CI) 0.50-0.99] and the use of more than two antihypertensive medications (AOR: 0.62, 95% CI 0.40-0.96) were associated with reduced odds of optimal BP control. Male sex (AOR: 1.75, 95% CI 1.14-2.70) and the use of renin-angiotensin-aldosterone system blocking medications (AOR: 2.07, 95% CI 1.18-3.64) were independently associated with proteinuria while DM (AOR: 1.69, 95% CI 1.06-2.55) and treatment with more than two medications (AOR: 1.86, 95% CI 1.09-3.17) were more likely to have reduced eGFR. CONCLUSION: A large proportion of hypertensive patients in north-central Nigeria have poorly controlled BP. Kidney damage is common among these patients.

Goodpasture's disease complicating human immunodeficiency virus infection.

Goodpasture's disease in association with human immunodeficiency virus (HIV) is rarely observed. Herein, we report a case of a 33-year-old Hispanic male who had both HIV and hepatitis C, and was subsequently diagnosed with autoantibodies to the glomerular basement membrane. On initial presentation he was anuric and hyperkalemic with an elevated creatinine. Hemodialysis was initiated, and a renal biopsy showed findings diagnostic of anti-glomerular basement membrane crescentic glomerulonephritis. Immunofluorescence microscopy showed strong (3+) linear staining of glomerular basement membranes by IgG, kappa; and lambda; light chains, and focal weaker staining of glomerular basement membranes for C3. Plasmapheresis, steroids and cyclophosphamide were all considered in treating this complex case. The patient received therapy with plasmapheresis and steroids during his initial hospitalization, but his renal function did not improve. He was discharged on hemodialysis 3 times per week. On a subsequent admission, the patient presented with symptoms and signs suggestive of pulmonary hemorrhage. Thus, plasmapheresis and cyclophosphamide were begun. His pulmonary symptoms improved with therapy, but he continued to require long-term hemodialysis. The development of Goodpasture's syndrome in a patient with HIV infection creates diagnostic and therapeutic dilemmas. The decision to treat the patient with immunosuppressive medications should lead to enhanced surveillance for infections.

Association between scleroderma, renal cell carcinoma and membranous nephropathy.

We report a patient with scleroderma, renal cell carcinoma (RCC) and membranous nephropathy (MN). Certain clinical and laboratory features suggested that RCC caused or enhanced the other two conditions. A 55-year-old man developed scleroderma which progressed rapidly during its first 2 years with development of hypertension and acute renal failure, peak serum creatinine (SCr) 327 micromol/l (3.7 mg/dl) and partial improvement of the renal function (SCr 239 micromol/l or 2.7 mg/dl) after initiation of an angiotensin converting enzyme inhibitor. He subsequently developed nephrotic syndrome (urine protein excretion 9 gm/24-h) and progressive renal failure, with SCr 469 +/- 18 micromol/l (5.3 +/- 0.2 mg/dl). An anti-nuclear mitotic apparatus protein (NUMA) antibody, which is uncommon in scleroderma but has been linked to certain malignancies, was found in his serum. A left upper pole RCC was removed by heminephrectomy. MN was found in the renal parenchyma adjacent to the excised tumor. In the 3.5 years following surgery, the clinical manifestations of scleroderma have been arrested while the medications prescribed for this condition have been greatly reduced. Proteinuria is consistently less than 1 gm/24-h and 42 months after surgery serum creatinine was 256 micromol/l (2.9 mg/dl). Nutrition has also improved. Although this case may represent chance occurrence of three uncommon diseases (scleroderma, RCC, MN) in the same individual, the sustained improvement of the manifestations of scleroderma and MN after resection of the RCC contrasted to the rapid course of these conditions until the surgery, and the presence in the patient's serum of an autoantibody which is uncommon in patients with scleroderma, but has been linked to malignancy, suggest a pathogenetic relationship between the three conditions.

Interleukin-6 modulates hepatic and muscle protein synthesis during hemodialysis.

Increased demand for amino acids to sustain acute-phase protein synthesis could be the stimulus for the increased muscle protein catabolism during hemodialysis (HD). This could be attenuated by intradialytic amino-acid infusion. To test this, we measured the fractional synthesis rates of albumin, fibrinogen, and muscle protein in eight patients with end-stage renal disease at baseline before dialysis and during HD without or with amino-acid infusion. The percentage change in the fractional synthesis rates of albumin, fibrinogen, and muscle protein from baseline was significantly higher during HD with amino-acid infusion than without amino-acid infusion. Leg muscle proteolysis was significantly increased during unsupplemented HD compared with baseline, but this was not decreased by amino-acid infusion. Arteriovenous balance studies across the leg showed a net efflux of interleukin-6 (IL-6) from the muscle into the vein during HD. The fractional synthesis rate of albumin, fibrinogen, and muscle protein correlated with each other and with the IL-6 efflux from the leg. Leg muscle protein catabolism was positively related to IL-6 release from the leg and not associated with amino-acid availability. Our results show that intradialytic cytokine activation and not amino-acid depletion is the major protein catabolic signal during HD.

Haemodialysis induces mitochondrial dysfunction and apoptosis.

BACKGROUND: Mitochondria play a crucial role in the regulation of the endogenous pathways of apoptosis activated by oxidant stress. Nuclear factor-kappaB (NF-kappaB) is a central integration site for pro-inflammatory signals and oxidative stress. MATERIALS AND METHODS: Peripheral blood mononuclear cells (PBMC) were isolated from eight end-stage renal disease (ESRD) patients before haemodialysis (Pre-HD) and during the last 10 min of HD (End-HD). A new polysulfone membrane (F70, Fresenius) was used for dialysis. Intracellular generation of reactive oxygen species (ROS), mitochondrial redox potential (Deltapsim) and PBMC apoptosis were determined by flow-cytometry. RESULTS: Plasma levels of interleukin-6 (IL-6) (24.9+/-7.0 vs. 17.4+/-5.5 pg dL(-1), P<0.05), IL-6 soluble receptor (52.2+/-4.9 vs. 37.6+/-3.2 ng dL(-1), P<0.02) and IL-6 gp130 (405.7+/-41.0 vs. 235.1+/-38.4 ng dL(-1), P<0.02) were higher end-HD compared to pre-HD. IL-6 secretion by the isolated PBMC (24.0+/-2.3 vs. 19.3+/-3.5 pg dL(-1), P<0.02) increased end-HD. Percentage of lymphocytes exhibiting collapse of mitochondrial membrane potential (43.4+/-4.6% vs. 32.6+/-2.9%, P<0.01), apoptosis (33.4+/-7.1% vs. 23.7+/-7.7%, P<0.01), and generation of superoxide (20.7+/-5.2% vs. 12.5+/-2.9%, P<0.02) and hydrogen peroxide (51.1+/-7.8% vs.38.2+/-5.9%, P<0.04) were higher at end-HD than pre-HD. NF-kappaB activation (3144.1+/-208.1 vs. 2033.4+/-454.6 pg well(-1), P<0.02), expression of B-cell lymphoma protein-2 (6494.6+/-1461 vs. 3501.5+/-796.5 ng mL(-1), P<0.03) and heat shock protein-70 (9.81+/-1.47 vs. 6.38+/-1.0 ng mL(-1), P<0.05) increased during HD. CONCLUSIONS: Intra-dialytic activation of cytokines, together with impaired mitochondrial function, promotes generation of ROS culminating in augmented PBMC apoptosis. There is concomitant activation of pathways aimed at attenuation of cell stress and apoptosis during HD.

Inadequacy of dialysis, chronic inflammation and malnutrition in Nigerian patients on chronic hemodialysis.

PURPOSE: To identify the extent of underdialysis, chronic inflammation and malnutrition and their interrelationships in Nigerian hemodialysis patients. METHODS: In a prospective study including 10 adult patients, (6 men, 4 women) on hemodialysis in North Central Nigeria, malnutrition was assessed by body mass index (BMI), serum albumin and prealbumin, and bioimpedance (BIA) pre-and post dialysis, inflammation was evaluated by C-reactive protein (CRP) and adequacy of dialysis was judged by frequency of the hemodialysis sessions and Kt/V urea. RESULTS: Post-dialysis BMI was 21.3 (19.9, 24.3) kg/m2 (< 20 kg/m2 in 4 patients), serum albumin 31.5 (24.0, 32.0) g/L (< 30.0 g/L in 5), serum pre-albumin 25.2 (15.3, 31.1) mg/dL (< 18.0 mg/dL in 4), serum CRP 4.8 (1.2, 11.5) mg/dL (> 1.0 mg/dL in 8), phase angle 4.2 (3.7, 5.1) degrees (< 3 degrees in 3) and body fat deficit was diagnosed by BIA in 4 patients. Weekly frequency of dialysis was 3 times in 2 patients, twice in 1 and 1.2 in one patient receiving dialysis only twice weekly). By combined frequency of dialysis and Kt/V urea values, no patient received an adequate dose of dialysis and, indeed, all patients had overt symptoms of uremia. Low body weight, low serological and BIA nutrition indices, and high CRP levels occurred in the same patients. Patients on dialysis for > 1 year had worse nutrition indices than those on dialysis for < 1 year. CONCLUSIONS: Underdialysis was universal, while poor nutrition and chronic malnutrition were found in the majority of the small number of patients studied. These three adverse conditions, which were interlinked, may be common in Nigerian hemodialysis patients, because their underlying socioeconomic causes are widespread.

Serum potassium and acid-base parameters in severe dialysis-associated hyperglycemia treated with insulin therapy.

We analyzed the changes in serum potassium concentration ([K]) and acid-base parameters in 43 episodes of dialysis-associated hyperglycemia (serum glucose level > 33.3 mmol/L), 22 of which were characterized as diabetic ketoacidosis (DKA) and the remaining 21 as nonketotic hyperglycemia (NKH). All episodes were treated with insulin therapy only. Age, gender, initial and final serum values of glucose, sodium, chloride, tonicity and osmolality did not differ between DKA and NKH. At presentation, serum values of [K] (DKA 6.2 +/- 1.3 mmol/L; NKH 5.2 +/- 1.5 mmol/L) and anion gap [AG] (DKA 27.2 +/- 6.4 mEq/L; NKH 15.4 +/- 3.5 mEq/L) were higher in DKA, whereas serum total carbon dioxide content [TCO2 ] (DKA 12.0 +/- 4.6 mmol/L; NKH 22.5 +/- 3.1 mmol/L), arterial blood pH (DKA 7.15 +/- 0.09; NKH 7.43 +/- 0.07) and arterial blood PaCO2 (DKA 26.2 +/- 12.3 mm Hg; NKH 34.5 +/- 6.7 mm Hg) were higher in NKH. At the end of insulin treatment, serum values of [K] (DKA 4.0 +/- 0.7 mmol/L, NKH 4.0 +/- 0.5 mmol/L), [AG] (DKA 16.3 +/- 5.4 mEq/L, NKH 14.9 +/- 3.0 mEq/L), [TCO2 ] (DKA 23.5 +/- 5.0 mmol/L, NKH 24.1 +/- 4.2 mmol/L), arterial blood pH (DKA 7.42 +/- 0.09, NKH 7.51 +/- 0.14) and arterial blood PaCO2 (DKA 31.8 +/- 6.7 mm Hg, NKH 34.2 +/- 8.3 mm Hg) did not differ between the two groups. Linear regression of the decrease in serum [K] value during treatment, (Delta[K]), on the presenting serum [K] concentration,([K]2 ), was: DKA, Delta[K] = 2.78 - 0.81 x [K]2 , r = -0.85, p < 0.001; NKH, Delta[K] = 2.44 - 0.71 x [K]2 , r = -0.90, p < 0.001. The slopes of the regressions were not significantly different. Stepwise logistic regression including both DKA and NKH cases identified the presenting serum [K] level and the change in serum [TCO2 ] value during treatment as the predictors of Delta[K] (R2 = 0.81). Hyperkalemia is a feature of severe hyperglycemia (DKA or NKH) occurring in patients on dialysis. Insulin administration brings about correction of DKA and return of serum [K] concentration to the normal range in the majority of the hyperglycemic episodes without the need for other measures. The initial serum [K] value and the change in serum [TCO2 ] level during treatment influence the decrease in serum [K] value during treatment of dialysis-associated hyperglycemia with insulin.

Lysosomal enzymes in preeclamptic women in northern Nigeria.

BACKGROUND: The incidence of preeclampsia is high in northern Nigeria, as it is in many other developing countries, and preeclampsia is associated with significant maternal and fetal morbidity and mortality. We inquired if proteinuria or hypertension alone could account for the altered concentrations of urinary lysosomal hydrolases that have been reported in preeclamptic women and pregnant women without preeclampsia. METHODS: The activities of urinary beta-hexosaminidase and beta-galactosidase were determined fluorometrically in pregnant women assigned to one of four groups: Group I: 41 preeclamptic women; Group II: 31 hypertensive aproteinuric women; Group III: 44 normotensive proteinuric women; and Group IV: 52 healthy pregnant women (controls). RESULTS: The urinary beta-hexosaminidase concentrations were decreased in the preeclamptic women (P<0.005) and proteinuric women (P<0.001) when compared to the healthy pregnant controls. There was no significant difference in beta-hexosaminidase concentrations between the hypertensive women and the healthy pregnant controls. The urinary beta-galactosidase concentrations for preeclamptic, hypertensive, and proteinuric women did not differ significantly versus healthy pregnant controls. CONCLUSIONS: The reduced urinary excretion of beta-hexosaminidase in preeclamptic women is associated with proteinuria, but not hypertension. Measuring urinary concentrations of lysosomal hydrolases alone or in conjunction with urinary protein concentrations is not likely to be useful in predicting or monitoring the clinical course of preeclampsia; however, it might prove important in gaining a more complete understanding of the pathogenesis of renal tubular epithelial cell injury and proteinuria that occurs in preeclampsia.

Serum tonicity, extracellular volume and clinical manifestations in symptomatic dialysis-associated hyperglycemia treated only with insulin.

The absence of osmotic diuresis modifies the effects of hyperglycemia on body fluids in patients with advanced renal failure. To determine the relationship between clinical manifestations and abnormalities in tonicity and extracellular volume in such patients, we analyzed 43 episodes of severe dialysis-associated hyperglycemia (serum glucose exceeding 600 mg/dL) treated only with insulin. The main manifestations were dyspnea in 22 cases (pulmonary edema in 19), nausea and vomiting in 15, coma in 13 and seizures in 3, while 5 patients had no symptoms. Treatment with insulin resulted in a decrease in serum glucose value from 913 +/- 197 mg/dL to 170 +/- 78 mg/dL, an increase in serum sodium level from 125 +/- 5 to 136 +/- 5 mmol/L, and a fall in calculated serum tonicity value from 300 +/- 13 to 282 +/- 11 mmol/kg (all at p < 0.001). The ratio of the change in serum sodium level over change in serum glucose concentration was -1.50 +/- 0.22 mmol/L per 100 mg/dL. The percent increase in extracellular volume secondary to hyperglycemia developing from the prior euglycemic state and calculated from changes in serum sodium and chloride concentrations, was 10.9% +/- 4.6% (1.5% +/- 0.6% per 100 mg/dL increase in serum glucose level). All clinical manifestations dissipated after correction of hyperglycemia in 42 patients. One woman developed during treatment a fatal myocardial infarction. Dialysis patients with severe hyperglycemia may develop symptoms as a result of hypertonicity and extracellular expansion. Insulin alone may be sufficient treatment for these symptoms. The changes in serum tonicity and electrolytes during treatment are consistent with theoretical predictions.

Neurological manifestations of uraemia and chronic dialysis.

BACKGROUND: The management of uraemic neurological manifestations is a major target of the treatment of the uraemic syndrome. Chronic dialysis is associated with novel neurological manifestations. OBJECTIVE: To describe the clinical characteristics, pathogenesis and management of the main neurological syndromes encountered in uraemia and chronic dialysis. METHODS: Review of the pertinent literature. Selected references, which have been critical in the understanding of the topic, were included in this review. RESULTS: The main neurological manifestations of uraemia include encephalopathy, neuropathy that can affect cranial, peripheral and autonomic nerves, and proximal myopathy. Retention of uraemic toxins is the main putative cause of uraemic encephalopathy and neuropathy. Arrest or prevention of uraemic encephalopathy and neuropathy are main targets of the dialytic treatment and constitute major criteria of its adequacy. The main cause of uraemic myopathy is secondary hyperparathyroidism and parathyroidectomy is its main treatment. Chronic dialysis is associated with three main neurological syndromes, the disequilibrium syndrome, seen usually in the first few haemodialysis sessions and prevented by starting dialysis with a low dose and progressively increasing the dialysis dose in subsequent dialysis sessions, dialysis dementia, which results from aluminium overloading and is prevented by reducing exposure of the dialysis patients to aluminium, and nerve entrapment, particularly carpal tunnel syndrome, which is caused by beta2-microglobulin amyloidosis and may be prevented by the use of high-flux dialysers which provide relatively high clearance for beta2-microglobulin or by daily haemodialysis. CONCLUSIONS: Specific neurological manifestations are part of the uraemic syndrome and may complicate chronic dialysis. The diagnosis of these manifestations, their differentiation from other neurological syndromes that can complicate the course of renal failure or dialysis, and their specific treatment require clinical acumen and represent a major challenge for physicians treating patients with chronic renal failure or undergoing chronic dialysis.

Severe proximal myopathy in advanced renal failure. Diagnosis and management.

Myopathies encountered in uremic patients may have different pathogenetic mechanisms and treatment. Secondary hyperparathyroidism may cause uremic myopathy responding to specific treatment. This study aimed at presenting a case illustrative of the clinical features, diagnosis and management of uremic parathyroid myopathy. A 66-year old man with renal failure from membranous nephropathy developed sensory signs of uremic neuropathy and progressive painless weakness of the pelvic girdle muscles bilaterally. Motor nerve conduction velocity was normal, electromyogram was consistent with a myopathic pattern, while muscle biopsy showed a pattern of atrophy more consistent with a neuropathic pattern. Serological tests for collagen vascular diseases and hyperthyroidism were negative, while serum muscle enzymes were not elevated and serum phosphate levels were not low. Serum parathyroid hormone level was grossly elevated, while serum calcium was mildly elevated in a small fraction of the measurements, serum alkaline phosphatase showed a progressive rise and skeletal bone survey did not disclose osteopenia or signs of parathyroid bone disease. A course of calcitriol failed to improve the myopathy, which responded promptly and dramatically to parathyroidectomy. Uremic parathyroid myopathy, which has a characteristic clinical picture, must be differentiated from other neuropathic or myopathic conditions that require specific treatments. Progressive parathyroid myopathy is, by itself, an indication for parathyroidectomy, which is curative in this case.

Chronic hemodialysis in a Nigerian teaching hospital: practice and costs.

The incidence of end-stage renal disease (ESRD) is on the rise in developing countries. To identify issues related to renal replacement therapy in ESRD patients in the developing world, we analyzed the practice and costs of hemodialysis in Nigerian ESRD patients. Ten ESRD patients were dialyzed at the Jos University Teaching Hospital, Jos, Plateau State, Nigeria, between June 15 and July 15, 2003. In these patients, we analyzed initiation, vascular access issues, frequency, duration, adequacy and economics of chronic hemodialysis. The Nigerian patients were referred to the nephrologist for the first time only when they had developed frank uremia. No patient had a permanent vascular access at the time dialysis was initiated. Only two patients had a functioning dialysis fistula, while the other eight patients were dialyzed through temporary femoral vein catheters that were removed after each dialysis. Frequency of dialysis was three times weekly in 2 patients, twice weekly in 1 patient and once weekly or less frequently in 7 patients. The duration of a dialysis session was prescribed to be 4 hours, but sessions often lasted for as long as 10 hours because of breakdowns of the antiquated dialysis machines. The urea reduction ratio was 45.3 +/- 8.6%. In every case, the cost of dialysis was borne by the patients and their families. Comparison of the cost of dialysis, with extensive re-use of supplies, to monthly incomes of Nigerians with different professions revealed that the great majority of Nigerians cannot afford three times weekly dialysis. Underdialysis in Nigerian ESRD patients is common and caused by socioeconomic factors and technologic deficits. One step towards correction of underdialysis could be sharing of the cost of dialysis by the public.

Oliguric acute renal failure in mycosis fungoides with lymphomatous infiltrates in the kidneys.

OBJECTIVE: To present the clinical picture of acute renal failure in patients with mycosis fungoides (MF) and renal lymphomatous infiltrates. To analyze the pathogenesis of renal failure. METHODS: Correlation of clinical picture, urinary findings, imaging reports and autopsy findings in two patients with long-standing MF who died with renal failure. CASE SUMMARIES: Both subjects had sustained oliguria in the last 2 weeks. One patient had persistent hypotension, normal urinalysis, normal renal sonogram, and scarce interstitial lymphomatous infiltrates with preservation of renal parenchymal architecture. He was thought to have ischemic acute renal failure not directly linked to the lymphomatous infiltrates. The second patient developed hypertension one month prior to death, and had moderate proteinuria, hematuria, pyuria, grossly enlarged kidneys with hypoechoic masses, and extensive replacement of the renal parenchyma by lymphomatous infiltrates. This picture is typical of renal failure secondary to lymphomatous replacement of the kidneys. CONCLUSIONS: The development of oliguric renal failure in MF with renal lymphomatous infiltrates may have varying clinical and imaging manifestations and pathogeneses. Potentially reversible pathogenic mechanisms should be systematically investigated, particularly if the overall clinical picture is not characteristic of renal failure secondary to lymphomatous replacement of the parenchyma.

Water and small solute excretion in continuous peritoneal dialysis patients with lean body mass exceeding 90% of body weight as estimated from creatinine kinetics.

Lean body mass computed from creatinine kinetics (LBM) is an index of somatic nutrition and correlates with other nutrition indices in CAPD. However, LBM exceeding 90% of body weight (LBM/W > or = 0.9) may be an index of non-compliance, rather than nutrition. To test this hypothesis, we analyzed fluid and solute excretion in 40 CAPD patients with LBM/W > or = 0.9 (group A). The comparison group (group B) consisted of 885 CAPD patients with LBM/W < 0.9. Group A was younger (38.3+/-14.8 vs 54.7+/-14.7 yr) and had a lower percent of women (23.5% vs 41.1%) and diabetic subjects (17.5% vs 42.6%) than group B (at P < or = 0.019). Group A also had lower body mass index (22.7+/-2.7 vs 25.8+/-5.1 kg/m2, P <0.001) and serum albumin (33.0+/-6.7 vs 35.2+/-5.5 g/L, P = 0.014). Despite similar prescribed daily fill volumes (group A 8.3+/-2.4, group B 8.5+/-2.2 L/24 h) and similar D/P urea and creatinine values, group A had higher daily drain volume (11.0+/-3.6 vs 9.6+/-2.1 L/24 h, P < 0.001). Renal clearances were similar, while peritoneal and total clearances were apparently higher in group A. Creatinine excretion was higher in group A (27.4+/-5.1 vs 13.6+/-4.1 mg/kg x 24 h, P < 0.001), with a large part of the excess creatinine excretion in group A being accounted for by peritoneal excretion. The combination of an apparently high daily ultrafiltration volume (2.7 L/24 h on the average), unrealistically high creatinine excretion rate, and relatively poor nutrition (low body mass index and serum albumin) in group A is consistent with non-compliance. We suggest that the finding of LBM/W > or = 0.9 during a clearance study in CAPD should trigger an investigation for non-compliance.

The relation between nutrition indices and age in patients on continuous ambulatory peritoneal dialysis receiving similar small solute clearances.

OBJECTIVE: To analyze the effect of age on nutrition indices in subjects on the same continuous ambulatory peritoneal dialysis (CAPD) schedule. METHODS: We analyzed 613 sets of clearance values and nutrition indices in 302 CAPD patients. Small solute clearances included urea clearance (Kt/Vurea) and creatinine clearance (Ccr). Nutrition indices included body mass index (BMI), serum albumin, urea and creatinine, 24-h urea nitrogen and creatinine excretion in urine plus dialysate, protein nitrogen appearance (PNA), PNA normalized by standard weight (nPNA), lean body mass (LBM) computed by creatinine kinetics, and LBM/Weight. CAPD subjects were classified in 4 age quartiles (Q): Group Q1, age 33.7 +/- 7.6 years, N = 149; group Q2, age 49.5 +/- 3.8 years, N = 158; group Q3, age 61.5 +/- 2.6 years, N = 154; and group Q4, age 72.1 +/- 5.4 years, N = 152. Group comparison was done by one-way ANOVA or chi-square. Predictors of low nutritional parameters were identified by logistic regression. Selected variables were compared by linear regression. RESULTS: Mean Kt/Vurea and Ccr were above the current adequacy standards and did not differ between the age quartiles. In contrast, older quartiles had, in general, lower nutrition indices than younger quartiles. However, the youngest quartile had the lowest BMI. By logistic regression, young age was a predictor of low BMI, while advanced age was a predictor of low creatinine and urea nitrogen excretion, low nPNA, and low LBM/Weight. The regressions of nPNA on Kt/Vurea differed between the age quartiles. By these regressions, the youngest quartile had higher nPNA values for the same Kt/Vurea than the oldest quartile in the clinically relevant range of Kt/Vurea and nPNA values. CONCLUSIONS: Nutrition indices are worse in older than in younger CAPD patients with the same small solute clearances. Nutrition of CAPD patients is adversely affected by age and requires special attention in the older age group.

Creatinine excretion in continuous peritoneal dialysis: a systematic error of the Cockroft-Gault formula.

We investigated the hypothesis that the rate of loss of creatinine excretion with age in peritoneal dialysis (PD) patients differs from the rate predicted from the Cockroft-Gault formula (Cr(Pred)) by analyzing creatinine excretion data obtained from clearance studies of 925 patients on continuous ambulatory PD therapy with an age range of 12 to 91 years. Measured creatinine generation (Cr(Meas)) is the sum of creatinine excretion in urine plus dialysate (Cr(Excr)) plus an estimated metabolic degradation of creatinine. The effect of age on Cr(Excr) and the differences Cr(Excr) - Cr(Pred) and Cr(Meas) - Cr(Pred) were analyzed by linear regression. In 373 women, Cr(Excr) = W(16.9360 - 0.084A), r = -0.342, P < 0.001 (where W is weight in kilograms and A is age in years). The regression slope was one half of the slope in the Cockroft-Gault formula. Cr(Excr) - Cr(Pred) = -413.91 + 4.78A, r = 0.300, P < 0.001. Cr(Meas) - Cr(Pred) = -176.36 + 4.37A, r = 0.278, P < 0.001. In 552 men, Cr(Excr) = W(21.079 - 0.108A), r = -0.338, P < 0.001. The regression slope was approximately one half of the slope in the Cockroft-Gault formula. Cr(Excr) - Cr(Pred) = -493.25 + 6.28A, r = 0.267, P < 0.001. Cr(Meas) - Cr(Pred) = -66.41 + 3.63A, r = 0.143, P = 0.001. The rate of loss of creatinine excretion with age is one half of the rate predicted by the Cockroft-Gault formula in both women and men on PD therapy. Therefore, the difference between excretion (or measured generation) of creatinine and creatinine generation predicted by the Cockroft-Gault formula is not constant, but increases with age. The Cockroft-Gault formula systematically overestimates the effect of age on creatinine excretion in PD patients and is not suitable for predicting creatinine excretion in these subjects.