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Abstract: The depleting fossil fuels with their ever increasing prices have paved ways for alternative fuels. Biodiesel is one of those alternative fuels which have picked up keen interest of the people due to its similar properties to diesel. However due to biodiesel being costlier than diesel in the present scenario, it has not been preferred to diesel. However if the cost of biodiesel is reduced then its effective usage can be made, either by blending with conventional diesel or by utilizing its byproduct (glycerol) effectively. One way is to use glycerol to produce hydrogen. Hydrogen, being another source of renewable energy, is also seen as a clean fuel for transportation purpose. Hydrogen can be prepared through glycerol via various routes namely steam reforming, auto-thermal reforming, partial oxidation, etc. The paper here focuses on the steam reforming process. This process is used widely used in the industries and it would not require much change in the system if the feedstock is changed to glycerol from naphtha or natural gas. However like every process this process also has some limitations which hinder the effective production of hydrogen. The paper throws light on these challenges, along with few possible solutions which can be used in order to avoid or eliminate these challenges and help in efficient production of hydrogen. [Copyright &y& Elsevier]

Experimental glomerulonephritis induced by heterologous GBM immunization in mice is temporarily prevented and reduced in severity when ATG is administered prior to or in conjunction with GBM. Once the disease is well established, ATG does not appear to significantly alter glomerular damage. [ABSTRACT FROM AUTHOR]

Mice immunized with dog glomerular basement membrane in Fruend's complete adjuvant uniformly developed severe renal lesions. A prominent event in many animals appeared to be mononuclear cell accumulation around small renal blood vessels. Glomerular lesions characterized by hypercellularity, thickening of basement membrane, necrosis, and well marked crescent formation were noted. Immunofluoresecnt and antibody elution studies from the kidneys of animals immunized with dog GBM demonstrated the presence of specific anti-GBM antibody which could be detected in mouse glomeruli 4 weeks after initial immunization. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine the effects of 4 months of exercise training (ET) on cardiorespiratory function and endurance, blood pressure, muscle strength, hematology, blood lipids, and renal function in individuals with chronic renal failure (CRF) who were not yet on dialysis. Sixteen subjects were recruited to volunteer for participation in this study, but only eight completed all study phases. Subjects were first evaluated before and after a 2-month baseline (BL1 and BL2), after 4 months of ET, and again after 2 months of detraining (DT). ET did not change hematology, blood lipids, or echocardiographic measurements of left ventricular function and mass. Resting systolic and diastolic blood pressures decreased significantly from BL after the ET (146 +/- 15.7/87 +/- 9 mm Hg to 124 +/- 17.5/78 +/- 9.5 mm Hg; P < 0.02), and then increased significantly after DT (139 +/- 14.7 mm Hg and 87 +/- 9.9 mm Hg; P < 0.01). Peak oxygen consumption (pVO2) changed significantly during the study (1.3 +/- 0.3 L/min, 1.5 +/- 0.3 L/min, and 1.4 +/- 0.3 L/min for BL2, ET, and DT, respectively; P < 0.02), as did the VO2 at the ventilatory threshold (0.65 +/- 0.18 L/min, 0.92 +/- 0.19 L/min, and 0.68 +/- 0.23 L/min for BL2, ET, and DT, respectively; P < 0.01). Knee flexion peak torque increased after ET (43.4 +/- 25.6 Nm to 51.0 +/- 30.5 Nm; P < 0.02). GFR, as measured by creatinine clearance, continued to deteriorate during the course of the study (25.3 +/- 12.0 mL/min, 21.8 +/- 13.2 mL/min, and 21.8 +/- 13.2 mL/min for BL2, ET, and DT, respectively; P < 0.001). Individuals with predialysis CRF who undergo ET improve in functional aerobic capacity, muscular strength, and blood pressure.

We investigated the predictors of serum albumin and the relationship between serum albumin and urea kinetic indices in continuous peritoneal dialysis (CPD). In a training set (TS) of 143 urea kinetic studies performed in 92 CPD patients, stepwise logistic regression identified high/high-average peritoneal solute transport, diabetes, advanced age and high daily drain volume normalized by body water as predictors of low serum albumin (< 35 g/liter). This analysis was then substantiated in a validation set (VS) of 187 kinetic studies performed in another 102 CPD patients. The calculated area under the receiver operating characteristic (ROC) curve by this logistic regression model was 0.782 (95% CI, 0.745 to 0.819). Logistic regression was repeated in the TS using only the first kinetic study from each patient, and it identified high/high-average peritoneal solute transport, diabetes, and advanced age as predictors of low albumin. Using only the first kinetic study from each patient in the VS, the second logistic regression model calculated an area under the ROC curve equal to 0.850 (95% CI, 0.810 to 0.890). The relative risk (RR) of serum albumin < 35 g/liter was computed for all kinetic studies after combining the TS and the VS and using non-diabetic CPD subjects aged < or = 61 years with low/low average peritoneal solute transport as the reference group. The RR with only one risk factor present ranged from 1.076 (age > 61 years) to 6.792 (high/high-average transport). The RR with two risk factors present ranged from 5.200 to 9.729. The RR with all three risk factors present was 9.100 (95% CI, range 3.923 to 21.111). A subset of 37 CPD patients had a second urea kinetic study 8 +/- 5 months after an increase in the amount of dialysis due to low urea clearance and/or uremic symptoms. The weekly KT/V urea increased from 1.40 +/- 0.24 to 2.10 +/- 0.31 after the increase in the CPD dose. With the increase in dialysis, the protein catabolic rate increased substantially; however, the mean serum albumin remained stable (from 33.9 +/- 4.6 to 33.3 +/- 6.2 g/liter; decrease 18; increase 15; same 4). In comparison to the subjects who had a decrease in serum albumin after the increase in KT/V, those with the increase in serum albumin were younger (44.2 +/- 11.2 vs. 54.3 +/- 16.2 years, P = 0.044) and had a higher serum urea after the increase in the dose of CPD (22.4 +/- 7.8 vs. 17.0 +/- 6.0 mmol/liter, P = 0.037). We conclude that the major predictors of low serum albumin in CPD are advanced age, diabetes, and high/high-average peritoneal solute transport, but not urea kinetic studies. An increase in the dose of dialysis does not cause a consistent rise in serum albumin in underdialyzed CPD subjects. However, a subset of younger patients may be able to increase their serum albumin in response to the increase in KT/V.

Objectives: To identify the most advantageous formula for estimating creatinine clearance (CCr) and to establish a dose of dialysis that will ensure minimal acceptable levels of creatinine clearance in patients on continuous peritoneal dialysis (CPD)., Design: Analysis of all CCr studies performed in CPD patients over 40 months., Setting: All four dialysis units following CPD patients in one city. One dialysis unit is government-owned, one is university-affiliated, and two are community based., Participants: One hundred and ninety-four patients representing almost the entire CPD population in Albuquerque., Interventions: Creatinine and urea clearance studies were performed in 24-hour urine and drained dialysate samples. Creatinine clearance (peritoneal plus urinary) was normalized to either 1.73 m2 body surface area (CCr) or body water estimated by the Watson formulas (KT/VCr). CCr and KT/VCr were either corrected by averaging urinary creatinine and urea clearances or were not corrected. Two dialysis units were designated as the training set (92 patients, 143 clearance studies) and the other two units as the validation set (102 patients, 181 clearance studies)., Main Outcome Measures: Minimal acceptable creatinine clearance levels were determined in the training set by computing the creatinine clearance value corresponding to 1.70 weekly KT/V urea by linear regression. Logistic regression models predicting low creatinine clearance were developed in the training set and were tested in the validation set., Results: The following weekly creatinine clearance values corresponded to 1.70 KT/V urea: corrected CCr 52.0 L/1.73 m2, uncorrected CCr 54.4 L/1.73 m2, corrected KT/VCr 1.46, uncorrected KT/VCr 1.53. Logistic regression identified as predictors of low creatinine clearance low daily urine volume (UV) and low daily dialysate drain volume/body water (DV/V) for all four creatinine clearance formulas, plus low/low-average peritoneal solute transport (only for uncorrected CCr) and serum creatinine (for both KT/VCr formulas). In the validation set, the predictive models produced an area under the receiver operating characteristic (ROC) curve between 0.835 and 0.919 indicating very good predictive accuracy. For corrected CCr and anuria, the regression model produced a minimal normalized drain volume (DV/V) value consistent with minimal acceptable CCr equal to 0.305 L/L per 24 hours. This DV/V cutoff detected low corrected CCR in validation set anuric subjects (n = 55) with a sensitivity of 85% and a specificity of 71%. For uncorrected CCR and anuria, DV/V cutoffs were 0.273 L/L per 24 hours (high/high-average peritoneal solute transport) and 0.420 L/L per 24 hours (low/low-average transport). Sensitivity and specificity of these cutoffs in validation set anuric subjects were 87% and 85%, plus 86% and 33%, respectively., Conclusions: The uncorrected CCr appears to be the most advantageous creatinine clearance formula in CPD, because it allows the use of peritoneal solute transport type in the calculation of the minimal required normalized drain volume. The minimal acceptable uncorrected CCr is 54.4 L/1.73 m2 weekly. To achieve this uncorrected CCr in anuria, the required minimal normalized drain volume is 0.273 L per liter of body water daily if peritoneal solute transport is high or high-average and around 0.420 L per liter of body water daily if peritoneal solute transport is low or low-average. The required total daily drain volume is computed by multiplying the required normalized drain volume by body water.

This study attempted to define the minimal dose of dialysis needed to produce a target KT/V in continuous peritoneal dialysis (CPD). In a training set of 143 clearance studies performed in 92 CPD patients, logistic regression identified low urine volume (UV) and low dialysate drain volume normalized by body water (DV/V) as predictors of weekly KT/V urea < or = 1.70. Solution of the regression equation with UV fixed at 0.00 1/24 h and at different probabilities of low KT/V provided a series of minimal DV/V values consistent with weekly KT/V > or = 1.70 in anuria. The accuracy of the logistic regression model and of the DV/V cut-offs was tested in a validation set (VS) of 189 urea kinetic studies performed in another 102 CPD patients. In the VS, the area under the Receiver Operating Characteristic curve generated by the regression model was 0.832 (95% Confidence Interval: 0.798-0.866). The DV/V cut-off value of 0.301 per 24 h, calculated by solving the regression model at p = 0.442 and with UV = 0, identified studies with weekly KT/V < 1.70 with a sensitivity of 89.3% and a specificity of 78.1% in anuric VS subjects (n = 60). Use of only the first urea kinetic study from each patient did not modify the predictors of KT/V or the cut-off values derived from solution of the regression model. The DV/V cut-off of 0.324 per 24 h, derived from the logistic regression model predicting KT/V < or = 1.90, identified KT/V < 1.90 in VS anuric subjects with a sensitivity of 94.3% and a specificity of 81.0%. Low UV and DV/V predict low KT/V urea in CPD. Prescribed 24 h exchange volume in anuric CPD subjects should be calculated to produce DV/V values exceeding 0.301 1/24 h per 1 body water for a KT/V of 1.70 and 0.324 1/24 h per 1 body water for a target weekly KT/V of 1.90.

Clinical and laboratory features and risk factors for diabetic gastroparesis (DGP) were investigated in 226 diabetics on chronic dialysis; 106 subjects (43%) had DGP diagnosed by persistent vomiting improved with the use of prokinetic agents and 120 (control group) had no clinical DGP. Type 1 diabetics had DGP more frequently than type 2 diabetics (70 vs. 37%). The DGP group had longer duration of diabetes (21 +/- 8 vs. 13 +/- 6 years), higher frequency of diabetic orthostatic hypotension (95 vs. 33%), enteropathy (49 vs. 5%), blindness (52 vs. 23%), myocardial infarction (86 vs. 42%), extremity gangrene (54 vs. 27%) and cerebrovascular accidents (43 vs. 25%), lower serum albumin 32.3 +/- 3.9 vs. 35.4 +/- 3.8 g/l), urea (24.0 +/- 5.5 vs. 25.5 +/- 5.5 mmol/l) and creatinine (710 +/- 210 vs. 820 +/- 220 mumol/l), and higher serum TCO2 (20.9 +/- 3.1 vs. 19.8 +/- 2.7 mmol/l) than the control group (all differences significant at p +/- 0.004). Glycemic control was adequate in 24% of the DGP group subjects and 83% of the control subjects (p < 0.001). Annual hospitalization rate was 49 +/- 48 days/patient in the DGP group and 16 +/- 27 days/patient in the control group (p < 0.001). Median patient survival was 24 +/- 2 months in the DGP group and 61 +/- 9 months in the control group (p < 0.0001). Logistic regression identified long duration of diabetes and poor glycemic control as risk factors for DGP. In diabetics on dialysis, DGP is associated with high frequency of other diabetic complications, low serum albumin and creatinine, and high morbidity and mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

This study was conducted to determine the association between glycemic control and clinical outcomes of diabetic patients maintained on chronic dialysis. The study group consisted of 226 diabetics (60 Type I and 166 Type II) classified as having either good glycemic control (> 50% of blood glucose determinations within 3.3-11.1 mmol/L) or poor glycemic control (< 50% of blood glucose measurements > 3.3 and < 11.1 mmol/L). The following variables were analyzed in each group: demographics; vascular and diabetic complications; laboratory values; and patient survival. In comparison to diabetics with poor control (Type I, n = 44; Type II, n = 57), those with good control, either Type I (n = 16), or Type II (n = 109), were dialyzed for longer periods and had shorter hospitalizations, lower prevalence rates of myocardial infarctions, congestive heart failure, orthostatic hypotension, gastroparesis and enteropathy, and higher mean serum albumin. Mean patient survival by life-table analysis was as follows: Type I diabetics, good control 128.9 + 8.1 months, poor control 29.5 + 5.0 months, p = 0.0014. Type II diabetics, good control 56.9 + 6.8 months, poor control 22.8 + 4.6 months, p < 0.0001. Good glycemic control during the first 6 months of dialysis predicted long-term survival for Type II but not for Type I diabetics. Poor glycemic control is associated with increased morbidity from vascular and diabetic complications, malnutrition, and shortened survival in diabetics on chronic dialysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetic control in 110 diabetics (39 type I and 71 type II), who had been on continuous ambulatory peritoneal dialysis (CAPD) for at least 3 months, was considered good (group G, n = 63) or poor (group P, n = 47) if > 50% or < or = 50% of glucose measurements, respectively, were within 3.3-11.1 mmol/L. Compared to group P, group G had more type I diabetics and fewer type II diabetics; higher serum cholesterol and lower serum creatinine; higher rates of blindness, autonomic neuropathy, congestive heart failure, myocardial infarction, cerebrovascular accidents and extremity gangrene; higher annual rates of peritonitis (1.47 +/- 1.31 vs 0.98 +/- 1.19 episodes/patient-year), exit-site/tunnel infection (0.83 +/- 1.14 vs 0.39 +/- 0.68 episodes/patient-year), and catheter loss (0.81 +/- 0.59 vs 0.39 +/- 0.52 episodes/patient-year); and longer hospitalization (38 +/- 31 vs 14 +/- 15 days yearly). All differences were significant at p = 0.05 or lower. According to life-table analysis, median patient survival was 25 +/- 3 months in group P and 85 +/- 17 months in group G (p < 0.0001). Technique survival was 14 +/- 2 months for group P and 28 +/- 4 months for group G (p < 0.0001). Good diabetic control in diabetics on CAPD is associated with better outcome and constitutes, therefore, a desirable therapeutic goal.

Eight diabetic men with poor glycemic control, probably worsened by severe congestive heart failure and gastroparesis, were sequentially dialyzed by CAPD and hemodialysis. Mean blood glucose concentration, blood glycosylated hemoglobin, and insulin dose were higher during CAPD than during hemodialysis. Among blood glucose determinations, however, the frequency of hypoglycemia (glucose less than 3.3 mmol/L) was higher during hemodialysis (13.2 +/- 8.9%) than during CAPD (2.8 +/- 2.1% p = 0.012), whereas the frequencies of hyperglycemia (glucose greater than 11.1 mmol/L) and euglycemia (glucose between 3.5 and 11.1 mmol/l) did not differ between the two dialysis modalities. Furthermore, hypoglycemia was severe during hemodialysis and was associated with two deaths. There were no deaths linked to abnormalities in blood glucose concentration during CAPD. When hypoglycemia is frequent in diabetics with poor glycemic control, CAPD is preferable to hemodialysis.

Technetium-99m DTPA renograms were performed before and after angioplasty in a 63-year-old man with bilateral renal artery stenosis (RAS), hypertension, and renal insufficiency. Decreased isotope uptake after captopril by the right kidney assisted in the selection of the right renal artery for angioplasty. Post-angioplasty improvement in both blood pressure control and renal function was accompanied by an absence of effect of captopril on the isotope uptake by the right kidney. In bilateral RAS, the captopril renogram is a useful tool for selecting the site for angioplasty, for assessing the adequacy of the procedure, and for long-term follow-up.

The authors analyzed the outcome of 56 episodes of cardiopulmonary resuscitation (CPR) in dialysis patients. Eleven patients (20%) left the hospital alive. Univariate analysis showed that a functional cause of cardiac arrest, absence of rib fractures, and the occurrence of cardiac arrest in the dialysis or intensive care units were associated with a favorable outcome. Logistic regression showed that the outcome of CPR was related to the presence of rib fractures, cause of arrest, degree of preexisting heart disease, and patient age. Despite the high incidence of rib fractures (77%), the outcome of CPR in dialysis patients is similar to its outcome in the general population.

Urokinase or streptokinase was instilled intraperitoneally as an adjunct to the antibiotic therapy in 16 episodes of relapsing or persistent peritonitis in CAPD patients. In eight patients the combination of antibiotics and intraperitoneal thrombolytic agents resulted in clearing of the infection with no recurrences. The treatment failed in eight other patients, who had their peritoneal catheters removed. Six of the last eight patients had either abdominal wall abscesses or persistence of the bacteria on the wall of the peritoneal catheter. Elevated post-intraperitoneal instillation peritoneal fluid neutrophil counts and positive post-instillation peritoneal fluid cultures predicted failure of the intraperitoneal instillation of thrombolytic agents in most instances. Intraperitoneal instillation of urokinase or streptokinase may help cure approximately 50% of the episodes of relapsing for persistent peritonitis. Post-instillation peritoneal fluid cell counts and cultures should be monitored. Radiologic investigation for abdominal wall or intraabdominal abscesses is indicated if intraperitoneal instillation of urokinase or streptokinase fails to eradicate peritonitis.

The morbidity and mortality of 11 femoral neck fractures were analyzed to compare operative and conservative management of femoral neck fractures in dialysis patients. All fractures occurred in older men with severe cardiac, pulmonary, gastro-intestinal, and neurologic conditions and with advanced renal osteodystrophy. Six of the seven operated patients survived the surgery and achieved varying degrees of ambulation. Stability of the operated hip was excellent in each case. Post-operative complications included transient confusional state related to narcotics, pneumonia, decubitus ulcers, and severe hypoalbuminemia. All four patients who were managed conservatively died from complications of the fracture. Progressive deterioration was noted in each nonoperated patient, with confusion caused by narcotics and analgesics, pneumonia, hepatic coma, decubitus ulcers, severe depression, and severe hypoalbuminemia. Therefore, operative management was superior to conservative management for femoral neck fractures of patients receiving chronic dialysis with multiple medical problems and advanced renal osteodystrophy. Narcotics must be used with great caution, and efforts should be directed toward prevention of malnutrition and decubitus ulcers.

Clinical course, complications and outcome were analyzed in 75 patients (14 women, 61 men) who started CAPD at age 55 years or older (55-81). These patients were separated in three groups. Group A patients had high risk for vascular disease (diabetes, hypertension, N = 45), group B patients had a presumed lower risk for vascular disease (primary renal disease, N = 22), and group C patients had miscellaneous conditions (N = 8). Group A was compared to group B. Patient and technique survival was statistically higher for group B than for group A. The rates of peritoneal dialysis related complications (peritonitis, tissue infections, catheter loss, hernias) were comparable between groups A and B. Hernias were seen frequently in all groups and had severe sequellae, including discontinuation of CAPD. Catastrophic vascular events were also seen in all groups, but the frequency of such events, particularly of catastrophic vascular events of the limbs, was statistically higher in group A than in group B. Vascular disease accounted for the majority of deaths in all groups. Four patients died from cardiovascular instability soon after changing from CAPD to hemodialysis. In conclusion, vascular disease is the major factor limiting survival in older CAPD patients. CAPD is superior to hemodialysis for a relatively small fraction of older patients with severe cardiovascular instability.

When serum glucose concentration is nearly normal, serum sodium concentration and tonicity are usually normal in ambulatory outpatient diabetics on chronic hemodialysis or peritoneal dialysis. In hyperglycemia, patients on hemodialysis do not undergo osmotic diuresis and are able to nearly normalize their serum tonicity by increasing the intake of water. Patients on peritoneal dialysis differ from hemodialysis patients because of continued loss of water in the peritoneal dialysate and achieve only partial correction of tonicity by water consumption. The model currently used to predict changes in serum sodium concentration and in tonicity from hyperglycemia assumes no changes in external balance of body water or solute during development of hyperglycemia and, therefore, is not applicable in ambulatory dialysis patients with intact thirst mechanism, because of water retention. In ambulatory patients on chronic dialysis, clinical manifestations of hyperglycemia include thirst, water intake, and weight gain. Neurologic manifestations due to hypertonicity are usually absent.

Anionic sites have been demonstrated in the basement membranes of peritubular capillaries. The anionic barrier function of peritubular capillary wall has been ascribed to these sites. Fenestrated capillaries in other organs have anionic sites in the endothelial cell glycocalyx and at the luminal surface of the fenestral diaphragms. The purpose of this study was to map anionic sites at the luminal surface of peritubular capillaries and to assess whether a concentration gradient for albumin exists across the endothelium. Partial chemical characterization of these anionic sites was done by in vivo enzymatic degradation. The difference in distribution of albumin following enzyme digestion was also studied. The binding of cationized ferritin to the luminal surface indicated that the rat peritubular capillaries have anionic sites along the entire luminal surface of the endothelial cell, including the fenestral diaphragms. Partial biochemical characterization of these sites shows that the sites in the glycocalyx are mainly from neuraminic acid, while the fenestral diaphragms have mainly heparan sulfate proteoglycans. Intravascular albumin extended to the endothelial luminal plasmalemma and to the luminal surface of fenestral diaphragms. Digestion with heparitinase was associated with the leakage of albumin outside the capillary wall. These findings suggest that the anionic surface of fenestrae constitutes a charge barrier of the peritubular capillaries.

Severe hyperkalemia (serum potassium level >6 mmol per liter [mEq per liter]), often with electrocardiographic disturbances, was noted at presentation in 30% of 73 hyperglycemic episodes (serum glucose concentration >25 mmol per liter [455 mg per dl]) observed in 15 in-hospital patients with insulin-dependent diabetes mellitus who were receiving long-term hemodialysis or peritoneal dialysis. Serum glucose concentration and total carbon dioxide content correlated significantly with the presenting serum potassium concentration. Treatment with parenteral insulin alone resulted in a decrease of the serum glucose value from 41 +/- 14 (standard deviation) to 11 +/- 5 mmol per liter (P <.001) and of serum potassium level from 5.2 +/- 1.2 to 4.0 +/- 0.6 mmol per liter (P <.001). The changes in serum glucose concentration and in carbon dioxide content and the serum potassium concentration at hyperglycemia were found to be independent correlates of the decrease in potassium concentration during treatment. Insulin alone resulted in correction of hyperkalemia in all instances. Posttreatment hypokalemia was noted in only two instances, each associated with both ketoacidosis and low-normal serum potassium concentration at hyperglycemia. Giving insulin is the only treatment usually needed for the hyperkalemia of hyperglycemia in patients on ongoing dialysis.

The anionic macromolecules at the glomerular endothelial cell surface are visualized only when stained with cationic stains. We investigated the arrangement and composition of this anionic matrix at the luminal surface. Rat kidneys were perfused with anionic ferritin (pI 4.5), ferritin (pI 7.4), or cationized ferritin (CF, pI 8.3). Anionic ferritin (pI 4.5) did not bind to the capillary wall, ferritin (pI 7.4) bound discontinuously only to the laminae rarae of the basement membrane, but cationized ferritin (CF, pI 8.3) bound as a thick continuous layer to the cell plasmalemma and bound to the anionic matrix in the fenestral spaces. These observations show that an anionic matrix lines the entire capillary lumen surface, fills the fenestrae, and is interposed between the blood and the basement membrane at the fenestrae. The anionic constituents at the capillary luminal surface were identified by in vivo digestion with specific enzymes. Absence of CF binding following digestion with specific enzymes was taken to indicate the presence of the particular glycoprotein known to be susceptible to the enzyme used. Neuraminidase digestion revealed that anionic sites over the surface plasmalemma are mainly from sialoproteins. In contrast, the matrix in fenestral channels contains heparan sulfate, hyaluronic acid, and sialoproteins. Papain digestion showed no glycolipids at the luminal surface. The functions of this continuous anionic layer located at the luminal surface of glomerular capillaries have not yet been established.

Renal blood flow in normal adults increases after protein ingestion. The mechanisms that create this hyperperfusion are unclear. A neurogenic factor in humans has not been definitively ruled out. Accordingly, we tested the hypothesis that a high-protein meal significantly increases renal blood flow to the denervated human kidney. We studied 11 transplant recipients (TR) with denervated kidneys and 4 kidney donors (KD) with a single innervated kidney. All subjects had normal urinalysis. Using noninvasive Doppler flowmetry that was previously validated, we determined renal blood flow (RQ, ml/min) after a 12-hr fast (F) and 1, 2, and 3 hr after a high-protein meal (500 ml) of 150 g protein, 30 g fat, and 30 g carbohydrate. The RQ (mean +/- SD, ml/min) at fasting and at 1, 2, and 3 hr postprandially was 409 +/- 100, 446 +/- 100, 493 +/- 122 (P less than 0.05 vs. F), and 500 +/- 123 (P less than 0.05 vs. F), respectively, for the TR, and was 654 +/- 60 (P less than 0.05 vs. TR), 667 +/- 86 (P less than 0.05 vs. TR), 776 +/- 80 (P less than 0.05 vs. F and TR), and 809 +/- 81 (P less than 0.05 vs. F and TR) for KD. We conclude that RQ in TR increases significantly after protein ingestion. Thus, in the noninstrumented, unanesthetized human with a transplanted kidney, neural control is not a factor in the increase in renal blood flow after a high protein meal.

A history of ingestion of large quantities of analgesics in patients having clinical and radiographic features of chronic interstitial nephritis leads to the diagnosis of analgesic nephropathy. In analgesic nephropathy the renal damage possibly occurs from a high concentration of analgesics and/or their metabolites. Since urinary concentrations of analgesics and their metabolites are also high, urinary bladder wall may be similarly damaged. Bladder urothelium was examined in 20 patients. Ten control patients with uremia, hypertension, or bladder neck obstruction showed normal histology. Two of the 5 patients with analgesic nephropathy had brownish pigmentation of bladder. All 5 analgesic nephropathy patients showed chronic inflammation similar to that found in 5 patients with bacterial infections. It is suggested that pigmentation of bladder wall and/or chronic inflammation of bladder mucosa of unknown etiology when found in a patient with chronic interstitial nephritis, would support the diagnosis of analgesic nephropathy.

The linearity and accuracy of noninvasive ultrasonic method of measuring beat-to-beat renal blood flow was evaluated by correlation with standard electromagnetic flowmetry. Using a combined real-time ultrasonic imager and pulsed Doppler velocimeter known as a duplex scanner (DS), lumen diameter (D) and average blood velocity (V) within the imaged renal artery were recorded. Renal blood flow ( QDS ) was calculated offline using a microprocessor from the equation QDS = (pi x D2 x V)/4. This noninvasive method had previously been validated in vitro using a controlled hydraulic system which modeled steady-state flow (QT) where QDS = 0.98 QT + 7.75, SEE = +/- 13.2, r = +0.98, P less than 0.001. In three anesthetized dogs, simultaneous QDS and electromagnetic flow ( QEMF ) measurements (range 44-484 ml x min-1) were made in the proximal left renal artery. Linear regression analysis gave QDS = 0.43 QEMF + 40.5, r = 0.78, SEE = 33.8 ml x min-1, P less than 0.01; QDS = 1.2 QEMF + 2.9, r = 0.86, SEE = 20.8 ml x min-1, P less than 0.01; QDS = 0.86 QEMF + 0.2, r = 0.93, SEE = 53.4 ml x min-1, P less than 0.01. These results suggest that noninvasive QDS measurements of renal blood flow are linear and reasonably accurate compared with invasive QEMF in dogs. The method may have utility in the noninvasive measurement of beat-to-beat blood flow in human renal arteries.

Previous micropuncture experiments have shown that gentamicin reduces the glomerular Kf even at low doses. Light and transmission electron microscopy have failed to provide evidence of structural alterations to explain the observed decreases in Kf. To elucidate and effects of gentamicin on glomerular ultrastructure, we used both scanning and transmission electron microscopy to study the glomeruli of rats given gentamicin at 4 and 40 mg/kg/day for 10 days, as well as 20 mg/kg/day for 4 weeks. Observations were also made during recovery from gentamicin-induced renal injury. Scanning and transmission electron microscopy revealed that gentamicin induced striking reductions in endothelial fenestral diameter, density, and area. These changes were not appreciated by light microscopy. By quantitative measurements, the reductions in endothelial fenestral area were found to be parallel to the previously observed reduction in Kf. During recovery, the morphological alterations improved pari passu with functional recovery. Contrary to observations in other models of acute renal failure, gentamicin-induced glomerular injury was unique in that the visceral epithelial surface was not affected. The mechanisms by which gentamicin induces alterations in glomerular ultrastructure remain to be defined.

In uranyl nitrate (UN)-induced acute renal failure (ARF) glomerular ultrafiltration coefficient (K(f)) decreases because of unknown reasons. Since transport of water across the glomerular capillary wall occurs predominantly extracellularly through the endothelial fenestrae (EF), a reduction in the diameter and/or the density of EF can reduce the extracellular filtration area and the glomerular K(f). To examine this possibility, ARF was induced in rats by intravenous administration of UN in low (15 mg/kg) and high doses (25 mg/kg). Fenestral density ( x+/-SEM) per 5 cm(2) from the scanning electron micrographs (x30,000) was 107+/-10, 103+/-9, and 101+/-11 at 2, 7, and 17 h after the intravenous administration of bicarbonate saline to the control rats. In the low-dose UN group the EF density was 91+/-2, 52+/-8, and 45+/-11 at 2, 7, and 17 h after the injection, whereas for the high-dose group at corresponding time intervals the EF density was 95+/-3, 54+/-9, and 44+/-10. Fenestral diameters, in Angstrom units ( x+/-SEM), were 751+/-53, 765+/-43, and 764+/-37 at 2, 7, and 17 h after the injection of bicarbonate saline to control rats. At corresponding intervals after the administration of UN, the fenestral diameters were 501+/-61, 472+/-28, and 438+/-98 for the low-dose group and 525+/-43, 470+/-39, and 440+/-56 for the high-dose group. 2, 7, and 17 h after the injection of UN, fenestral area of the low-dose group decreased to 52.1, 30.1, and 24.6% of the controls, whereas in the high-dose group, the fenestral area declined to 54.3, 30.2, and 23.6% of the controls. Administration of UN (15 mg/kg) to sodium-loaded rats did not alter renal function or endothelial cell morphology. It is suggested that in UN-induced ARF the morphological alterations in endothelial cells reduce the K(f) of glomerular capillaries by reducing the filtration area.

The abnormal cutaneous flora of hemodialysis (HD) patients might contribute to their frequent septic complications. We compared the effects of 13 wk of Betadine and 13 wk of Hibiclens on the skin flora of HD patients and personnel. Skin cultures were obtained weekly immediately prior to the disinfection, preceding each triweekly HD treatment, and monthly, at 2 and 4 hr postdisinfection. Total bacterial counts from predisinfection cultures were not significantly altered over either 13-wk treatment period. Hibiclens reduced total bacterial counts (p less than 0.01) and eradicated cutaneous staphylococci (p = 0.032) at both 2 and 4 hr postdisinfection significantly more than did Betadine. No reduction of staphylococcal sensitivity to either germicidal agent could be demonstrated. Neither agent was associated with severe adverse reactions and Hibiclens could not be detected in the blood. Hibiclens appears to offer short-term advantages over Betadine in the HD setting because of significantly longer duration of antibacterial activity.

The authors studied hyperglycemia occurring in insulin-dependent diabetic patients on chronic dialysis to determine the types of associated acid-base disorders, their treatment, and any differences from hyperglycemia in diabetic patients with intact renal function. Eighty-eight episodes of serum glucose greater than 25 mmol/L were observed, 23 in hemodialysis patients and 65 in patients on continuous peritoneal dialysis. Treatment consisted of low-dose insulin in 77 episodes and low-dose insulin plus saline in 11; no base was administered. Seventeen episodes (19%) presented with ketoacidosis. Arterial blood gas determinations were carried out at presentation in 37 of the episodes without ketoacidosis. Of these, 12 had respiratory alkalosis, six had respiratory acidosis and severe pulmonary edema, 14 had other single or mixed acid-base disorders, and only five had normal acid-base status. Insulin corrected the ketoacidosis in all instances and both pulmonary edema and respiratory acidosis in five of six instances. In eight cases metabolic alkalosis developed during treatment, without external acid loss. At the completion of treatment respiratory alkalosis was present in half the cases. No difference was noted between patients treated with hemodialysis or peritoneal dialysis. Insulin alone is sufficient for the management of hyperglycemia in dialysis patients. Certain acid-base disorders persist, but do not need further treatment. Hyperglycemia in patients on dialysis is characterized by infrequent development of metabolic acidosis and frequent presentation with respiratory alkalosis, by respiratory acidosis that is corrected by insulin, and by metabolic alkalosis developing during treatment without external cause.

Noninvasive characterization of renal artery blood flow variables in the human has not been reported. Using a unique dual-frequency real-time two-dimensional echo Doppler (Duplex scanner) that was calibrated in vitro, we characterized renal artery blood flow patterns in 16 normal subjects (6 females). Calculated mean values of systolic diameter (Ds), maximal spatial average blood velocity (Vmsa), and volume flow rate (Q) were as follows: 4.5 +/- 0.6 mm right, 4.4 +/- 0.6 mm left; 67.6 +/- 9.4 cm . sec-1 right, 69.6 +/- 12.0 cm . sec-1 left; and 403 +/- 127 ml . min-1 right, 395 +/- 98 ml . min-1 left; respectively. Direct linear regression correlation of body surface area (BSA) with Ds and Q were statistically significant (P less than 0.01, r = 0.70; and P less than 0.01, r = 0.72, respectively). In a blind prospective series, six of seven angiographically normal renal arteries were noninvasively identified by normal geometry and blood velocity patterns. One angiographically normal artery was incorrectly classified as mildly stenotic. Eleven angiographically documented abnormal renal arteries were noninvasively identified by their abnormal blood flow patterns and/or geometry. This study suggests that dual-frequency Duplex scanning with careful sample volume control and Doppler audio spectra/blood velocity waveform analysis can be used to characterize blood flow variables in normal and diseased human renal arteries.

Fourteen episodes of peritonitis complicating chronic peritoneal dialysis were treated with intravenous injections of 1 gm of vancomycin weekly for 4 successive weeks. Peak (one hour after completion of injection) and trough (immediately before the next injection) serum and dialysate vancomycin levels were measured. Vancomycin treatment resulted in a cure in 12 episodes (85.7%). Serum vancomycin levels were always above therapeutic range, but did not rise, with subsequent injections, to toxic range. Dialysate vancomycin levels were therapeutic for more than 85% of the measurements. One patient, who failed to respond to vancomycin plus cephalosporins, was cured with intraperitoneal streptokinase plus the same antibiotics. In another patient, a relapse was cured with vancomycin plus oral rifampin. Dialysate vancomycin levels were therapeutic in the last two patients. Peritoneal catheters were not removed. No significant side effects of vancomycin treatment were observed.

We evaluated the diagnostic accuracy of ultrasonic echo-Doppler velocimetry for the noninvasive diagnosis of renal artery stenosis. Renal artery stenosis was diagnosed if one or more of the following four abnormal hemodynamic parameters were found by Doppler velocimetry: (1) peak blood velocity greater than 100 cm . sec-1 in a focal area along the length of a renal artery, (2) absence of blood velocity during diastole, (3) absence of any detectable blood velocity denoting occlusion, or (4) broad-band Doppler frequency spectra due to focal blood velocity disturbances. With these criteria, the presence or absence of renal artery stenosis was blindly evaluated in 26 patients (52 arteries) who underwent standard or digital subtraction angiography. Compared to arteriography (reduction in diameter greater than or equal to 50%), the sensitivity of Doppler method was 89%, while its specificity was 73%. This noninvasive method may be useful in selecting patients for radiographic evaluation of renal artery stenosis and in the long term follow-up of these patients. Furthermore, echo-Doppler velocimetry may have the unique capability of assessing the hemodynamic consequences of renal artery stenosis.

Five patients, one woman and four men, aged 24 to 54 years, developed abnormally high hematocrits between 4 and 22 months after renal transplantation. In four patients, red cell mass was above normal and plasma volume below normal. In one patient, both red cell mass and plasma volume were below normal. The cause of the deranged plasma volume was not evident. Decreased plasma volume may either contribute to or may, in rare instances, be the only cause of apparent erythrocytosis in renal transplant recipients.

Nine of 81 members of two families were found to have renal problems. Three patients in one family had renal-retinal dysplasia with probable recessive inheritance. Of the 6 patients in the second family, one received a kidney transplant from his brother who initially had no detectable renal abnormality but later developed renal failure. In this family, the mode of inheritance seems to be dominant. Hereditary renal-retinal dysplasia differs from medullary cystic disease and nephronophthisis in its pattern of uniformly recessive inheritance and its accompaniment by retinitis pigmentosa. Because genetic considerations have important implications in selection of donors for renal transplant, these entities should be considered distinct despite the similarities in their clinical and pathologic features.

We analyzed causes and clinical associations of hemodialysis performed during the course of CAPD in 71 patients (34 diabetic) on CAPD between 1978 and 1988. Thirty seven patients had at least one hemodialysis during CAPD. Causes (multiple for some patients) included poor compliance with CAPD (20 patients), peritoneal catheter loss from infection (16 patients), and miscellaneous other conditions (18 patients). Hemodialysis rates were similar between diabetic and non-diabetic CAPD patients. Compared to non-hemodialyzed patients, CAPD patients hemodialyzed for poor compliance had higher rates of peritonitis (one episode per 8.3 patient months vs one episode per 23.4 patient months, p less than 0.001) and catheter loss (one loss per 27.7 patient months vs one loss per 112.0 patient months, p less than 0.001), and exhibited a trend towards more deaths (annual mortality 30.9% vs 14.3%, p = 0.067). Hemodialysis performed in CAPD patients because of poor compliance is associated with higher rates of peritonitis and catheter loss, and, probably, with increased mortality.