Jen-Tse Cheng

Course and prognosis of human immunodeficiency virus-associated nephropathy

PURPOSE Patients infected with the human immunodeficiency virus (HIV) have been described to have an unusual form of renal disease known as HIV-associated nephropathy. This condition is characterized by severe proteinuria, rapid progression to renal insufficiency, and a morphologic pattern of focal segmental glomerulosclerosis (FSGS) on renal biopsy. Despite increasing awareness of this entity, the epidemiology and clinical course of HIV-associated nephropathy are not yet well defined. We therefore decided to study HIV-infected patients with this biopsy-proven pattern of focal sclerosis. PATIENTS AND METHODS Using life-table analysis, we evaluated the clinical features and course of 26 patients with HIV infection and biopsy-proven FSGS and compared them with those in 24 subjects with HIV infection who had no glomerular disease at autopsy. RESULTS The group with FSGS had a higher percentage of blacks (96% versus 46%) and intravenous drug abusers (42% versus 17%), and had a higher mean serum creatinine level (5.4 mg/dL versus 1.0 mg/dL) than the group of HIV-infected subjects without glomerular disease. At the time of diagnosis of FSGS, six patients had clinical acquired immunodeficiency syndrome (AIDS), eight had AIDS-related complex (ARC), and 12 patients had no evidence of AIDS or ARC. The progression to end-stage renal disease for all patients was rapid, with a median time to dialysis of 10.9 weeks. Duration of patient survival was dependent upon the stage of HIV infection at the time of diagnosis of renal disease. Patients who presented with AIDS had a median survival of 1.9 months, compared to a median survival of 3.6 months for those with ARC and 9.7 months for initially asymptomatic HIV carriers (p less than 0.05). Fifteen patients either presented with or developed AIDS during the course of the study, and all died as a consequence of their immunodeficiency. Survival curves from the diagnosis of AIDS to death were similar in the group with HIV-associated nephropathy (7.3 weeks) compared to the control AIDS group without renal disease (6.9 weeks). CONCLUSION Our data indicate that FSGS associated with HIV infection can occur before other manifestations of AIDS, is more common in blacks and in intravenous drug abusers, and is rapidly progressive to uremia. Patient survival is dependent upon the stage of HIV infection. These findings may prove useful in devising more effective strategies for the care of this growing patient population.

Acute bilateral renal infarction secondary to cocaine-induced vasospasm

CASE PRESENTATION A 47-year-old African-American male with a history of hypertension for 1 year and cocaine use presented to the emergency department with acute onset of bilateral flank pain, nausea, vomiting, and diarrhea. Physical examination was unremarkable. Laboratory evaluation revealed a white blood count of 15.1 K/μl (normal 4.5-11.5 K/μl) and a serum creatinine of 2.4mg/100ml. A non-contrast CT scan of the abdomen was unremarkable. The patient was treated with morphine (for pain) and i.v. fluids, felt better, and was discharged for out-patient follow-up. The patient saw his primary care physician 2 days later (day 3) and reported persistence of the bilateral flank pain. The patient also reported a transient inability to urinate for 36 h before the visit. An abdominal ultrasound and blood chemistry were obtained. On day 5, he was referred by his physician to the emergency department for a serum creatinine of 9.2 mg/100 ml from day 3. At the time of admission, the patient reported using 5-6g/day of ibuprofen for the previous 4 days and admitted to sniffing cocaine a few hours before the initial onset of flank pain. On physical examination, the patient was a well-built African-American male with a temperature of 99.2 °F, pulse rate of 60/min, blood pressure of 150/85 mm Hg and weight of 85 kg (BMI 27.7 kg/m 2 ). There was no orthostasis, pallor, or skin rash. The heart and lung examinations were unremarkable. The abdomen was soft, with no suprapubic dullness. There was no costovertebral angle tenderness or pitting edema. The extremity pulses were symmetric and equal. Laboratory results are presented in Table 1. Serologic tests for hepatitis B and C viruses, human immunodeficiency virus, antinuclear antibody, and rheumatoid factor were negative. Serum complements, including C3, C4, and CH50, were within the normal range. Hemoglobin electrophoresis, chest X-ray, electrocardiogram, and echocardiogram were unremarkable. Renal ultrasound revealed normal-sized kidneys with mildly increased echogenecity and no hydronephrosis. A 99m Tc-MAG3 (mercaptoacetyltriglycine) radionuclide renogram showed multiple wedge-shaped photopenic areas in both kidneys (Figure 1a). Owing to the absence of a clear explanation for the patients acute renal failure, renal biopsy was performed 12 days after the onset of symptoms.

The Case ∣ 41-year-old HIV patient with proteinuria and progressive renal dysfunction

A 41-year-old patient was referred with proteinuria and a recent rise in serum creatinine from 1 to 1.5 mg/dl. The patient’s history was significant for recurrent alcoholic pancreatitis and a myocardial infarction 8 years earlier when he was diagnosed to be HIVand hepatitis B-positive. The patient had a history of nocturia for 5 years and frothy urine for 1 year but denied any diarrhea. His medication regimen for the past 4 years consisted of emtricitabine, tenofovir, atazanavir, and ritonavir (for HIV and Hepatitis B coinfection) as well as enalapril and atenolol. Physical examination was unremarkable and his blood pressure was 104/65 mm Hg. Laboratory studies showed (in mmol/l) Na 143, K 3.8, Cl 110, CO2 21, and a BUN 18 mg/dl, blood pH of 7.349, blood glucose of 92 mg/dl, serum phosphate 2.4 (reference range: 2.7–4.5 mg/dl), uric acid 3.6 (reference range: 3.6–7.7 mg/dl), normal complement levels and negative ANA, ANCA and rheumatoid factor. Urinalysis by dipstick showed a pH 5.0, 1þ protein, 1þ blood, and 1þ glucose. A 24-h urine collection (3 l) had 1.86 g of protein, 0.34 g of albumin, and 1.9 g creatinine. Serial laboratory tests are shown in Table 1. Urine sediment microscopy performed on the day of the renal biopsy showed 0–1 RBC, 0–1 WBC, 4–5 renal epithelial cells (some cigar shaped)/high-power field (Figure 1), with 5–6 fine granular casts/low-power field. No oval fat bodies or eosinophils were identified. Kidneys were normal in size and echotexture on ultrasonography.

Identifying Hemodialysis Catheter Recirculation Using Effective Ionic Dialysance

Vascular catheter use for dialysis remains highly prevalent, however, it is frequently adversely affected by access recirculation (AR). We previously reported the utility of effective ionic dialysance (EID)/blood flow rate (Qb) ratio in identifying significant (>5%) AR in arteriovenous (AV) fistulas (Mohan et al ASAIO J 56:427–433, 2010). We present data from 58 patients, receiving hemodialysis via venous catheters (85% tunneled cuffed catheters) who underwent intermittent monitoring for AR with the saline dilution technique (Transonic HD02 monitor) and had EID and Qb measurements from Diascan biosensor in the Gambro Phoenix dialysis machine available. Among the 193 hemodialysis sessions studied, 74 instances of significant access recirculation (sAR) were identified. A higher incidence of sAR occurred with temporary catheters and catheters in the femoral vein. We report a significant correlation between the EID/Qb ratio and AR in addition to demonstrating the predictive utility of the ratio for identifying dysfunction catheters with sAR (area under the receiver operator characteristic curve of 0.86 with a sensitivity of 79% and a specificity of 76% at an EID/Qb ratio of ⩽ 0.60). Our data demonstrate the utility of the EID/Qb ratio as an indicator of sAR in dialysis catheters albeit at a different threshold than that seen with AV fistulae.

Influence of concomitant prednisolone on trimethoprim-associated hyperkalaemia

OBJECTIVES Trimethoprim-sulfamethoxazole may cause hyperkalaemia by the amiloride-like effect of trimethoprim on sodium channels in the distal nephron. Hyperkalaemia usually occurs after 7-10 days and has been reported in 20%-50% of patients receiving trimethoprim-sulfamethoxazole. Patients with Pneumocystis jiroveci pneumonia and severe hypoxaemia benefit from the use of prednisolone as an adjuvant to trimethoprim-sulfamethoxazole. The addition of prednisolone may lower the incidence of trimethoprim-related hyperkalaemia due, in part, to its mineralocorticoid activity. We studied the effect of concomitant prednisolone on trimethoprim-related hyperkalaemia. PATIENTS Thirty patients qualified for inclusion and were reviewed. Patients were divided into two groups: one group received trimethoprim-sulfamethoxazole plus prednisolone (18 patients); and the other group received trimethoprim-sulfamethoxazole alone (12 patients). RESULTS The two groups were comparable at baseline, except for the severity of the P. jiroveci pneumonia. Hyperkalaemia developed in seven patients: all in the prednisolone and trimethoprim-sulfamethoxazole group. The greater incidence of hyperkalaemia in this group is surprising and was counter to our expectation. CONCLUSIONS Although it is possible that there is an unexplained interaction between trimethoprim and prednisolone, we postulate that our observation is a result of the catabolic effect of prednisolone. The patients treated with trimethoprim-sulfamethoxazole plus prednisolone appear to be more likely to develop hyperkalaemia than patients treated with trimethoprim-sulfamethoxazole alone.