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PubMed1984

Glomerular alterations in uranyl acetate-induced acute renal failure in rabbits.

The study was performed to elucidate the progression and regression of superficial and inner glomerular alterations in uranyl acetate-induced renal failure in rabbits. Fifteen hours after the drug injection, creatinine clearance (CCr) decreased to 55% of controls with slightly elevated plasma creatinine concentration (initiation stage). After 5 days, urine flow and CCr decreased to approximately zero, with severe azotemia (maintenance stage). Scanning electron microscopic observations in these stages revealed a flattening and spreading of podocyte cell bodies associated with loss of epithelial foot processes, and reduction in the density of endothelial fenestrae. These changes were more advanced in the maintenance stage. Glomerular and fenestral diameters did not significantly change in the initiation stage but increased in the maintenance stage. There was no significant difference in these morphologic alterations, however, between the superficial and inner glomeruli. Glomerular alterations reverted to normal within 14 days, with good recovery of glomerular function. The findings show no significant difference in the progression or regression of the glomerular changes between the superficial and deep cortex. These morphologic changes may play a role in the reduction of CCr observed in this model.

Acute Kidney Injury↗
PubMed1985

Course of acute renal failure studied by a model of creatinine kinetics.

A computerized model of creatinine kinetics was developed to predict the relationship between creatinine clearance [G(t)] and plasma creatinine concentration [C(t)] in patients with postischemic acute renal failure (ARF). A comparison of predicted to measured values in 35 episodes of ARF in 27 patients revealed three patterns of declining G(t) following an ischemic insult. Pattern A, characterized by an abrupt step decrement in G(t) following an isolated renal ischemic episode lasting minutes or hours, was observed in nine patients. It was followed invariably by an immediate ramp increment in G(t), despite which C(t) continued to increase for several days. Urinary indices during the period of increasing azotemia were consistent with the resolving stage of ARF. Patterns B (N = 15) and C (N = 11) were associated with persistent renal ischemia of long (days to weeks) duration and were respectively characterized by prolonged ramp or exponential decrements in G(t). A concurrent increase in C(t) was associated with urinary indices typical of the maintenance or sustained stage of ARF. Recovery of G(t) was observed in only two-thirds of patterns B and C cases and took the form of a ramp or exponential increment. Because G(t) and total body water were changing rapidly in ARF, changes in measured plasma creatinine levels alone failed to identify these patterns of deteriorating or improving renal function. However, when the computerized model was used in conjunction with daily measured values of C(t) and body weight and occasional estimates of G(t), the course and prognosis of ARF in individual patients were illuminated.

Acute Kidney Injury↗
PubMed1986

Peritoneovenous shunt in the management of the hepatorenal syndrome.

The hepatorenal syndrome (HRS) is a terminal complication of severe liver disease associated with a mortality of 80 to 90%. Although the renal functional abnormalities in the HRS suggest prerenal azotemia, volume expansion with saline, albumin or ascitic fluid rarely results in reversal of the HRS because fluid redistributes from the vascular space. Since the peritoneovenous (PV) shunt causes sustained central volume expansion, it has been advocated for the treatment of the HRS. We prospectively compared the PV shunt (N = 10) to Medical Therapy (MED) (N = 10) on renal function and mortality in 20 patients with the HRS associated with alcoholic liver disease. The HRS was diagnosed on the basis of clinical, hemodynamic, and laboratory criteria. The insertion of a PV shunt resulted in an increase in pulmonary capillary wedge pressure (4.2 +/- 1.1 vs. -1.5 +/- 1.0 mm Hg, P less than 0.01) and in cardiac index (0.8 +/- 0.3 vs. -0.2 +/- 0.3 1/min/m2, P less than 0.05). After 48 to 72 hours, weight (+3.1 +/- 1.1 kg) and serum creatinine (3.9 +/- 0.5 to 5.5 +/- 0.7 mg/dl, P less than 0.001) were increased with MED therapy and decreased (weight: -3.7 +/- 0.7 kg; serum creatinine: 3.6 +/- 0.4 to 3.0 +/- 0.5, P less than 0.05) with the PV shunt. Despite improvement in renal function, only one patient with the PV shunt had prolonged survival (210 days). In the remainder, survival was 13.8 +/- 2.2 days compared to 4.1 +/- 0.6 days with MED therapy. We conclude that the PV shunt often stabilizes renal function, but does not prolong life in patients with the HRS.

Adult↗
PubMed1987

Comparison of loop diuretics in patients with chronic renal insufficiency.

Furosemide and bumetanide share a number of characteristics including reduced natriuretic effects in azotemic patients. It has been presumed that this condition affects each drug equally. Previous studies, however, suggest dissimilar pathways of delivery to their sites of action. Though not rigorously tested, this potential disparity might cause them to differ when used in azotemia. We, therefore, assessed the pharmacokinetic and pharmacodynamic characteristics of intravenously administered furosemide and bumetanide in ten adult patients with stable, chronic renal insufficiency (mean creatinine clearance = 14.1 +/- 2.0 ml/min/1.73 m2) in a randomized, cross-over study during controlled sodium intake. Our goals were to assess differences in diuretic effectiveness and in so doing to determine the dose required to produce a maximal response. The mean diuretic doses of 172 and 4.3 mg for furosemide and bumetanide, respectively (ratio = 40:1) were sufficient to produce a maximum response. Despite similarities in maximal fractional excretion of sodium (18.2 +/- 2.6% with furosemide vs. 19.4 +/- 4.5% with bumetanide, P = 0.687) demonstrating an equal tubular responsiveness to both drugs, overall response as quantified by cumulative natriuresis in the initial eight hour period was 52% greater with furosemide (108 +/- 17 vs. 71 +/- 7 mEq; P = 0.042). The difference in total excreted sodium was accounted for by a preserved nonrenal clearance of bumetanide (113 +/- 12 compared to 53 +/- 5 ml/min for furosemide, P = 0.001) which resulted in relatively less bumetanide in serum available to be delivered into the urine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

A focus of tissue necrosis increases renal susceptibility to gentamicin administration.

The purpose of this study was to determine whether a retained focus of necrotic tissue predisposes to aminoglycoside-induced acute renal failure (ARF). Rats were subjected to either (1) 25% liver ligation, creating a focus of ischemic tissue which was left in place; (2) 25% liver resection; or (3) sham liver ligation. Gentamicin, 80 mg/kg bid, was administered for two days after surgery to all three groups. A fourth group was subjected to 25% liver ligation but no gentamicin therapy. Only rats subjected to partial liver ligation plus gentamicin treatment developed ARF, manifested by azotemia (BUN 80 +/- 2; creatinine 1.63 +/- 0.21; mg/dl) and tubular necrosis. This occurred in the absence of any discernible reduction in arterial blood pressure, renal blood flow, excessive weight loss, or ascites formation. The partial liver ligation-gentamicin group had 70% higher renal gentamicin concentrations than the liver resection-gentamicin controls (P = 0.01). To assess whether factors released from necrotic liver might account for these findings, additional rats were infused with: (1) 1 ml of a soluble liver extract alone; (2) 1 ml of liver extract plus gentamicin; or (3) 1 ml of saline plus gentamicin. Only the liver extract/gentamicin group developed ARF (BUN 88 +/- 13; creatinine 1.46 +/- 0.25). This occurred in association with a 110% increase in renal gentamicin uptake (P less than 0.03). In separate experiments, 5 ml liver extract infusions caused ARF (BUN 118 +/- 7; creatinine 2.1 +/- 0.18) without gentamicin treatment. In conclusion, a focus of liver necrosis can predispose to experimental gentamicin nephrotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1992

Response of cortical collecting ducts from remnant kidneys to arginine vasopressin.

Chronic renal failure is associated with impaired urine concentration. Previous studies have demonstrated that cortical collecting ducts (CCD) from uremic rabbits (with remnant kidneys) have an impaired response to arginine vasopressin (AVP). To determine whether this defect is an early, integral component of compensatory renal growth by the remnant kidney, we studied the response of CCD derived from rabbits one week after 75% nephrectomy. At one week, hypertrophy and adaptation in sodium transport are fully developed, but azotemia and interstitial fibrosis are absent. The animals with remnant kidneys failed to respond normally to water deprivation and dDAVP (maximum urine osmolality 738 +/- 29.1 mOsm/kg compared to 1378 +/- 207 in sham operated). However, in isolated, perfused CCD from remnant kidneys, AVP stimulated hydraulic water permeability to the same extent as in normal CCD or CCD from sham operated animals. AVP-induced cAMP generation per mm tubule length was significantly higher in the CCD from remnant kidneys (137.4 +/- 14.5 fmol/mm) than in the control group (82.4 +/- 11.9 fmol/mm), but not different when expressed per micrograms protein. These studies demonstrate that one week after reduction in renal mass there is no defect in the response of CCD to AVP, suggesting that the mechanisms responsible for the hyposthenuria after loss of renal mass are not related to any intrinsic cellular changes that occur in CCD early during compensatory renal growth.

Animals↗
PubMed1992

Mild renal ischemia activates primed neutrophils to cause acute renal failure.

The role of neutrophils (PMN) in acute renal failure (ARF) is controversial. Although the development of acute renal failure (ARF) frequently occurs in situations where there is partial activation of PMN (primed PMN) and mild renal ischemia, the interaction between primed PMN and ischemic organs has not been studied in any biological system. To define the interaction between primed PMN and mild renal ischemia, kidneys were made ischemic for 10 minutes in situ and reperfused by the isolated kidney technique with untreated PMN or PMN primed with low concentrations of lipopolysaccharide (LPS) or phorbol myristate acetate (PMA). We found that primed PMN had no effect on control (non-ischemic) kidneys and that untreated PMN did not cause injury to kidneys previously subjected to mild ischemia. However, addition of primed PMN to mildly ischemic kidneys caused severe injury. To determine the nature of renal injury, ischemic kidneys were reperfused with primed PMN and catalase (CAT) or the elastase inhibitor, Eglin C. In ischemic kidneys reperfused with LPS-primed PMN, Eglin C (but not CAT) was partially protective while in ischemic kidneys reperfused with PMA-primed PMN, CAT (but not Eglin C) was partially protective. Reperfusion with both CAT and Eglin C completely prevented the damaging effects of either LPS- or PMA-primed PMN. In conclusion, addition of primed but not untreated PMN causes ARF in mildly ischemic kidneys by PMN oxidant- and/or protease-mediated mechanisms. This synergism could account for the high frequency of ARF in conditions associated with prerenal azotemia and primed PMN.

Acute Kidney Injury↗
PubMed1994

Responses to hemorrhagic arterial pressure reduction in different ischemic renal failure models.

Renal blood flow (RBF) autoregulation has been found to be impaired in both norepinephrine (NE) and renal artery clamp (RAC) rat ischemic acute renal failure models. However, the decline in RBF at the normal lower limit of autoregulation is greater in NE-ARF. The present study was designed to determine if this difference in autoregulatory profiles has potential functional and morphologic significance. After demonstrating a fall in RBF to renal perfusion pressure reduction to 90 mm Hg that was twofold more in one week NE- than RAC-ARF (p < 0.001), separate rats of both ischemic ARF types with nearly identical levels of azotemia and glomerular filtration rate reduction and sham-ARF rats were subjected to four-hour controlled reduction in mean arterial pressure to 90 by transient phlebotomy at one week. On day 9, two days after mean arterial pressure reduction, blood urea nitrogen (BUN), serum creatinine (SCr) and creatinine clearance (CCr) showed continued improvement in RAC-ARF, but there were significant increases in BUN (46 +/- 22 to 72 +/- 10 mg/dl) and SCr (1.2 +/- 0.2 to 1.5 +/- 0.2 mg/dl) and a decline in CCr (0.434 +/- 0.127 to 0.334 +/- 0.079 ml/min) in the NE-ARF group (all P < 0.02). The mean sum of scores of morphologic indices of ARF was higher in NE- than RAC-ARF kidneys of rats sacrificed on day 9 but interstitial edema was the only individual index that was worse in NE-ARF.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1995

Progression of overt nephropathy in non-insulin-dependent diabetes.

The detection of overt albuminuria (> 300 mg/g creatinine) in the absence of azotemia was used to diagnose early nephropathy in 34 Pima Indians with NIDDM of 16 +/- 1 years duration. Differential solute clearances were performed serially to define the course of the glomerular injury over 48 months. At baseline, the GFR (107 +/- 5 ml/min), filtration fraction and sieving coefficients of relatively permeant dextrans (< 52 A) were all depressed below corresponding values in 20 normoalbuminuric Pima Indians with a similar duration of NIDDM. Over the ensuing 48 months the GFR (-34%) and filtration fraction (-13%) in the nephropathic patients declined further. The sieving coefficients of large, nearly impermeant dextrans (> 56 A radius) increased selectively and fractional clearances of albumin and IgG increased correspondingly by > 10-fold. Analysis of the findings with pore theory revealed: (1) a progressive decline in pore density and the ultrafiltration coefficient (Kf); and (2) broadening of glomerular pore-size distribution that resulted in greater prominence of large pores (> 70 A radius). We conclude that increasing loss of intrinsic ultrafiltration capacity is the predominant cause of the early and progressive decline in GFR that follows the development of nephropathy in NIDDM. We speculate that progressive impairment of barrier size-selectivity contributes to but does not fully account for the increasingly heavy proteinuria that is observed early in the course of this disorder.

Adolescent↗
PubMed2000

Solitary hepatic abscess with associated glomerulonephritis in a neonate.

A full-term neonate with a history of umbilical venous catheterization followed by coagulase-negative staphylococcal sepsis is presented. The infant developed a solitary hepatic abscess with saprophytic organisms. Her liver abscess resulted in acute glomerulonephritis characterized by hypertension, proteinuria, oliguria, and azotemia. Surgical drainage and antibiotic treatment of the abscess was associated with resolution of the glomerulonephritis. Glomerulonephritis due to solitary liver abscess in a neonate has not been reported previously. Acute onset of glomerulonephritis should prompt a search for occult sources of infection.

Abscess↗
PubMedDate not supplied

Improved fluid management utilizing humidified incubators in extremely low birth weight infants.

OBJECTIVE: To compare fluid and electrolyte management in extremely low birth weight (ELBW) infants nursed in humidified versus nonhumidified incubators. STUDY DESIGN: Setting--tertiary intensive care nursery. Subjects--all infants with birth weight < 1000 g admitted 1/95 to 1/99 who were treated with incubators and survived for > 96 hours (N = 155). Intervention--retrospective comparison of daily weights, fluid intakes, urine outputs, and serum electrolytes between group 1 (n = 70, nonhumidified incubators, born 1/95 to 1/97) and group 2 (n = 85, humidified incubators, born 1/97 to 1/99) over the first 4 days after birth. RESULTS: Despite similar daily weight losses between groups, group 1 infants received higher fluid intakes, had lower urine outputs, and had a higher incidence of hypernatremia, hyperkalemia, and azotemia (p < 0.05). Although no differences in mortality or the incidence of patent ductus arteriosus, bronchopulmonary dysplasia, or the overall rate of nosocomial infections were observed, the proportion of gram-negative isolates increased significantly (62%, p < 0.05) following the introduction of humidified incubators. CONCLUSIONS: ELBW weight infants nursed in humidified incubators have lower fluid requirements, improved electrolyte balance, and higher urine outputs during the first 4 days after birth compared to those nursed in nonhumidified incubators.

Bronchopulmonary Dysplasia↗
PubMed2006

Morphometric evidence for impairment of renal autoregulation in advanced essential hypertension.

A morphometric study was performed on 22 renal biopsies from hypertensive patients with proteinuria and/or azotemia, with no evidence of other renal disease. These results were compared with our earlier study of normotensive aging kidneys. Afferent arterioles in hypertensive kidneys showed a significant increase in lumen diameter (15.7+/-4.9 vs 13.4+/-4.7 microm, P=0.0007) and wall area (1234+/-769 vs 998+/-445 microm(2), P=0.037), due primarily to shift in the distribution of arteriolar types, from predominantly normal toward predominantly hyaline arterioles in hypertension. Glomeruli were divided into four basic types: normal, hypertrophic, focal segmental glomerulosclerosis (FSGS) type, and sclerosing. Overall, glomeruli in hypertensive kidneys were much larger than in normotensive aging kidneys, for example, total capillary area (16 247+/-10 681 vs 11 624+/-5702 microm(2), P<0.00001). This increase was due primarily to an increase in size of each type, for example, for hypertrophic glomeruli: total capillary area (22 205+/-10 426 vs 15 349+/-4577 microm(2), P=0.0038). There was an excellent correlation between arteriolar lumen diameter and mean glomerular capillary area for hypertrophic/FSGS-type glomeruli (r=0.4778, P=0.0013), such that as arteriolar diameter increases the mean glomerular capillary area increases, consistent with loss of autoregulation. The morphologic correlates of loss of autoregulation, with afferent arteriolar dilatation and increase in glomerular capillary size, glomerular hypertrophy, and subsequent FSGS, are present on a focal basis in aging kidneys and, much more extensively, although still focally, in hypertensive kidneys.

Adult↗
PubMed2006

Naïve and central memory T-cell lymphopenia in end-stage renal disease.

End-stage renal disease (ESRD) is associated with increased propensity to infections, diminished response to vaccination, impaired cell-mediated immunity, and reduced CD4+/CD8+ T-lymphocyte ratio. Four subsets of CD4+ and CD8+ T cells have been recently identified: naïve cells (as yet uncommitted), central memory (CM) cells (previously programmed), and CD45RA-positive and CD45RA-negative effector memory (EM) cells (programmed to perform specific effector functions). The effect of ESRD on subpopulations of T lymphocytes is unclear and was studied here. Twenty-one hemodialysis patients and 21 age-matched controls were studied. Pre- and post-dialysis blood samples were obtained and analyzed by three-color flow cytometry. CD4+/CD8+ ratio and the numbers of the naïve and CM CD4+ and CD8+ T cells were significantly reduced, whereas the numbers of EM CD4+ and CD8+ T cells were unchanged in the ESRD group. The reduction of the naïve and CM T-cell counts in the ESRD group was associated with increased apoptosis of these cells. Negative correlations were found between severity of azotemia, oxidative stress, and hyperphosphatemia with the number of naïve T cells. Comparison of diabetic with non-diabetic ESRD patients revealed higher numbers of total CD8+ cells and EM CD8+ T cells in the diabetic group. Dialysis did not significantly change the naïve and CM CD4+ or CD8+ cell counts, but significantly lowered CD8+ EM cell count. Thus, ESRD results in increased apoptosis and diminished populations of naïve and CM T lymphocytes. This phenomenon may, in part, contribute to the impaired immune response in this population.

CD4-Positive T-Lymphocytes↗
PubMed2006

Cardiorenal effects of celecoxib as compared with the nonsteroidal anti-inflammatory drugs diclofenac and ibuprofen.

The cardiorenal safety database from the Celecoxib Long-term Arthritis Safety Study (CLASS) was analyzed to examine whether supratherapeutic doses of celecoxib are associated with decreased renal function and blood pressure (BP) effects compared with standard doses of diclofenac and ibuprofen in osteoarthritis (OA) and rheumatoid arthritis (RA) patients.In total, 8059 patients were enrolled; 7968 received at least one dose of study drug (RA: N = 2183; OA: N = 5785). Patients received celecoxib, 400 mg twice a day (b.i.d.). (N = 3987); ibuprofen, 800 mg three times a day. (N = 1985); or diclofenac, 75 mg b.i.d. (N = 1996). Effects measured included: investigator-reported hypertension, edema or congestive heart failure, clinically important BP elevations, incidence of patients starting new antihypertensive medication, and increases in serum creatinine or reductions in creatinine clearance. Celecoxib was associated with a similar incidence of hypertension or edema to diclofenac but significantly lower than ibuprofen. The celecoxib group had significantly fewer initiations of antihypertensives versus ibuprofen. Systolic BP increases of >20 mmHg and above 140 mmHg occurred significantly less often with celecoxib compared with ibuprofen or diclofenac. Changes in serum creatinine or estimated creatinine clearance occurred in a similar percentage of patients taking celecoxib or ibuprofen; modest differences were evident against diclofenac. In patients with mild prerenal azotemia, significantly fewer patients taking celecoxib exhibited clinically important reductions in renal function (3.7%), compared with diclofenac (7.3%; P < 0.05) and ibuprofen (7.3%; P < 0.05). A supratherapeutic dose of celecoxib was associated with an improved cardiorenal safety profile compared with standard doses of either ibuprofen or diclofenac.

Acid-Base Equilibrium↗
PubMed2006

Exosomal Fetuin-A identified by proteomics: a novel urinary biomarker for detecting acute kidney injury.

Urinary exosomes containing apical membrane and intracellular fluid are normally secreted into the urine from all nephron segments, and may carry protein markers of renal dysfunction and structural injury. We aimed to discover biomarkers in urinary exosomes to detect acute kidney injury (AKI), which has a high mortality and morbidity. Animals were injected with cisplatin. Urinary exosomes were isolated by differential centrifugation. Protein changes were evaluated by two-dimensional difference in gel electrophoresis and changed proteins were identified by mass spectrometry. The identified candidate biomarkers were validated by Western blotting in individual urine samples from rats subjected to cisplatin injection; bilateral ischemia and reperfusion (I/R); volume depletion; and intensive care unit (ICU) patients with and without AKI. We identified 18 proteins that were increased and nine proteins that were decreased 8 h after cisplatin injection. Most of the candidates could not be validated by Western blotting. However, exosomal Fetuin-A increased 52.5-fold at day 2 (1 day before serum creatinine increase and tubule damage) and remained elevated 51.5-fold at day 5 (peak renal injury) after cisplatin injection. By immunoelectron microscopy and elution studies, Fetuin-A was located inside urinary exosomes. Urinary Fetuin-A was increased 31.6-fold in the early phase (2-8 h) of I/R, but not in prerenal azotemia. Urinary exosomal Fetuin-A also increased in three ICU patients with AKI compared to the patients without AKI. We conclude that (1) proteomic analysis of urinary exosomes can provide biomarker candidates for the diagnosis of AKI and (2) urinary Fetuin-A might be a predictive biomarker of structural renal injury.

Acute Kidney Injury↗
PubMed2003

Comparison of dipyridamole and fosinopril on renal progression in nephrectomized rats.

There is evidence to suggest that antiplatelet aggregation and inhibition of angiotensin converting enzyme will attenuate the progression of renal disease. In the present study, dipyridamole (DPM; 30 mg/kg per day, p.o.) or fosinopril (FOS; 20 mg/kg per day, p.o.) was given to rats for 5 weeks starting immediately after renal mass reduction (right uninephrectomy and ligation of approximately two-thirds of the blood supply to the left kidney). Renal mass reduction caused increased mean arterial blood pressure, reduced effective renal plasma flow (ERPF) and glomerular filtration rate (GFR), azotemia and proteinuria. Neither proteinuria nor hypertension was affected by DPM, although renal function improved markedly. Rats receiving FOS showed normalization of blood pressure with a significant increase in both ERPF and GFR, along with a lower degree of proteinuria. A histological examination of the remnant kidney detected the presence of vasodilation with a lower degree of podocyte swelling in both treatment groups, with a remarkable effect in the FOS group. These data indicate that both FOS and DPM attenuate the progression of glomerular disease associated with renal mass reduction in rats. However, FOS was more beneficial than DPM because it reduced proteinuria and lowered blood pressure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

Regional citrate anticoagulation in continuous venovenous hemofiltration in critically ill patients with a high risk of bleeding.

BACKGROUND: Systemic heparinization is associated with a high rate of bleeding when used to maintain patency of the extracorporeal circuit during continuous renal replacement therapy (CRRT) in critically ill patients. Regional anticoagulation can be achieved with citrate, but previously described techniques are cumbersome and associated with metabolic complications. METHODS: We designed a simplified system for delivering regional citrate anticoagulation during continuous venovenous hemofiltration (CVVH). We evaluated filter life and hemorrhagic complications in the first 17 consecutive patients who received this therapy at our institution. Blood flow rate was set at 180 ml/min. Ultrafiltration rate was maintained at 2.0 liters/hr and citrate-based replacement fluid (trisodium citrate 13.3 mM, sodium chloride 100 mM, magnesium chloride 0.75 mM, dextrose 0.2%) was infused proximal to the filter to maintain the desired fluid balance. Calcium gluconate was infused through a separate line to maintain a serum-ionized calcium level of 1.0 to 1.1 mM. RESULTS: All patients were critically ill and required mechanical ventilation and vasopressor therapy. Systemic heparin anticoagulation was judged to be contraindicated in all of the patients. A total of 85 filters were used, of which 64 were lost because of clotting, with a mean life span of 29.5 +/- 17.9 hours. The remaining 21 filters were discontinued for other reasons. Control of fluid and electrolyte balance and azotemia was excellent (mean serum creatinine after 48 to 72 hr of treatment was 2.4 +/- 1.2 mg/dl). No bleeding episodes occurred. Two patients, one with septic shock and the other with fulminant hepatic failure, developed evidence for citrate toxicity without a significant alteration in clinical status. Nine patients survived (52.9%). CONCLUSION: Our simplified technique of regional anticoagulation with citrate is an effective and safe form of anticoagulation for CVVH in critically ill patients with a high risk of bleeding.

Adult↗
PubMed1999

HIV-associated nephropathy is a late, not early, manifestation of HIV-1 infection.

BACKGROUND: Human immunodeficiency virus-associated nephropathy (HIVAN) can be the initial presentation of HIV-1 infection. As a result, many have assumed that HIVAN can occur at any point in the infection. This issue has important implications for appropriate therapy and, perhaps, for pathogenesis. Since the development of new case definitions for acquired immunodeficiency syndrome (AIDS) and better tools to assess infection, the relationship of HIVAN to the time of AIDS infection has not been addressed. In this study, we reassessed the stage of infection at the time of HIVAN diagnosis in 10 patients, and we reviewed all previously published cases applying the new case definitions to assess stage of infection. METHODS: HIVAN was confirmed by kidney biopsy in HIV seropositive patients with azotemia and/or proteinuria. CD4+ cell count and plasma HIV-1 RNA copy number were measured. We also reviewed all published cases of HIVAN to determine if AIDS-defining conditions, by current Centers for Disease Control definitions, were present in patients with biopsy-proven HIVAN. RESULTS: Twenty HIV-1 seropositive patients with proteinuria and an elevated creatinine concentration were biopsied. HIVAN was the single most common cause of renal disease. CD4+ cell count was below 200/mm3 in all patients with HIVAN, fulfilling Centers for Disease Control criteria for an AIDS-defining condition. HIV-1 plasma RNA was detectable in all patients with HIVAN. In reviewing previous reports, an AIDS-defining condition was present in virtually all patients with HIVAN. CONCLUSION: HIVAN develops late, not early, in the course of HIV-1 infection following the development of AIDS. This likely accounts for the poor prognosis noted in previous publications and has implications for pathogenesis. In addition, given the detectable viral RNA levels, highly active antiretroviral therapy is indicated in HIVAN. Highly active antiretroviral therapy may improve survival as well as alter the natural history of HIVAN.

AIDS-Associated Nephropathy↗