Biomedical subjects

Ravinder K Wali

Publications and source records attributed to Ravinder K Wali.

7 recordsLinked to original sources

PubMed2006

Acute renal failure and nephrotic range proteinuria due to amyloidosis in an HIV-infected patient.

Amyloidosis is an uncommon cause of renal disease in HIV-positive patients. Diagnosis is challenging, treatment options are limited, and prognosis remains poor. We discuss an HIV-positive patient with acute renal failure and nephrotic range proteinuria. The differential diagnosis included nephropathy due to trimethoprim/sulfamethoxazole, tenofovir, HIV, hepatitis C, heroin, or multifactorial causes. Serum and urine study findings were inconclusive. Rapid clinical deterioration ensued and a renal biopsy was performed. Pathologic examination revealed eosinophilic, amorphous material in the glomerular tufts that stained red-orange with Congo red stain. Immunohistochemical analysis confirmed amyloid A (AA) amyloidosis. AA amyloidosis occurs as a complication of chronic infection or chronic inflammatory disease. It has been reported in intravenous or subcutaneous drug abusers, some of whom were HIV-positive. This case underscores the importance of tissue diagnosis to determine the cause of renal disease in HIV-positive patients. Clinical diagnosis, based on CD4 count, viral load, and degree of proteinuria, may not predict the pathological diagnosis in HIV-positive patients.

Acute Kidney Injury↗

PubMed2005

Effect of kidney transplantation on left ventricular systolic dysfunction and congestive heart failure in patients with end-stage renal disease.

OBJECTIVES: We examined the impact of kidney transplantation on left ventricular ejection fraction (LVEF) in end-stage renal disease (ESRD) patients with congestive heart failure (CHF). BACKGROUND: The ESRD patients with decreased LVEF and a poor New York Heart Association (NYHA) functional class are not usually referred for transplant evaluations, as they are considered to be at increased risk of cardiac and surgical complications. METHODS: Between June 1998 and November 2002, 103 recipients with LVEF < or =40% and CHF underwent kidney transplantation. The LVEF was re-assessed by radionuclide ventriculography gated-blood pool (MUGA) scan at six and 12 months and at the last follow-up during the post-transplant period. RESULTS: Mean pre-transplant LVEF% increased from 31.6 +/- 6.7 (95% confidence interval [CI] 30.3 to 32.9) to 52.2 +/- 12.0 (95% CI 49.9 to 54.6, p = 0.002) at 12 months after transplantation. There was no perioperative death. After transplantation, 69.9% of patients achieved LVEF > or =50% (normal LVEF). A longer duration of dialysis (in months) before transplantation decreased the likelihood of normalization of LVEF in the post-transplant period (odds ratio 0.82, 95% CI 0.74 to 0.91; p < 0.001). The NYHA functional class improved significantly in those with normalization of LVEF (p = 0.003). After transplantation, LVEF >50% was the only significant factor associated with a lower hazard for death or hospitalizations for CHF (relative risk 0.90, 95% CI 0.86 to 0.95; p < 0.0001). CONCLUSIONS: Kidney transplantation in ESRD patients with advanced systolic heart failure results in an increase in LVEF, improves functional status of CHF, and increases survival. To abrogate the adverse effects of prolonged dialysis on myocardial function, ESRD patients should be counseled for kidney transplantation as soon as the diagnosis of systolic heart failure is established.

Female↗

PubMed2005

Chronic kidney disease: a risk factor for cardiovascular disease.

The goal of risk stratification of CVD inpatients with CKD is to lead to effective and early intervention and to prevent the adverse outcomes associated with this complex multisystem disease that is characteristic of growing number of patients with CKD in the general population and of patients receiving dialysis therapy or kidney transplantation. By 2030, there will be 2.24 million patients with ESRD in the United States, and approximately 1.3 million of these cases of ESRD will be caused by diabetes mellitus. Thus, CVD in this high-risk population presents a challenge for the nephrology and the cardiology community.

Cardiovascular Diseases↗

PubMed2004

BK virus-associated nephropathy in renal allograft recipients: rescue therapy by sirolimus-based immunosuppression.

BACKGROUND: BK virus nephritis (BKN) in recipients of renal allografts has reemerged during the past 5 years. Despite increased incidence, therapeutic options remain limited and progression of the disease often leads to allograft failure. METHODS: From May 2002 to July 2002, we performed protocol biopsies in 25 recipients of kidney allografts with progressive allograft dysfunction; three patients demonstrated unexpected histopathologic features of BKN. We tested the hypothesis that replacement of their lymphocytotoxic and nephrotoxic immunosuppression (combination of mycophenolate and tacrolimus) with sirolimus- and prednisone-based therapy can lead to disappearance of the virus without increasing the risk of acute rejection. RESULTS: During the median follow-up of 18 months after sirolimus and prednisone therapy, decoy cells disappeared first, followed by progressive decrease in the median plasma BK virus-DNA load, and undetectable levels at the last follow-up. Patients remained free of acute rejection, and follow-up median estimated creatinine clearance increased to 67 mL/min (range 62-75 mL/min) from 52 mL/min (range 51-54 mL/min) at the time of diagnosis. CONCLUSIONS: Further studies are needed, but at present these preliminary results offer a new direction for therapeutic intervention in recipients of renal allografts with BKN.

Adult↗

PubMed2004

Retransplantation in patients with graft loss caused by polyoma virus nephropathy.

The characteristics and outcome in 10 patients who underwent retransplantation after losing their renal grafts to BK virus-associated nephropathy (BKAN) are described. The patients underwent retransplantation at a mean of 13.3 months after failure of the first graft. Nephroureterectomy of the first graft was performed in seven patients. Maintenance immunosuppression regimens after the first and second grafts were similar, consisting of a combination of a calcineurin inhibitor, mycophenolate mofetil, and prednisone. BKAN recurred in one patient 8 months after retransplantation, but stabilization of graft function was achieved with a decrease in immunosuppression and treatment with low-dose cidofovir. After a mean follow-up of 34.6 months, all patients were found to have good graft function with a mean creatinine of 1.5 mg/dL. From this collective experience from five transplant centers (although the follow-up after retransplantation was not extensive), it can be concluded that patients with graft loss caused by BKAN can safely undergo retransplantation. The risk of recurrence does not seem to be increased in comparison with the first graft.

Adult↗

PubMed2002

Recent developments in toxic nephropathy.

Toxic nephropathy is an important cause of reversible renal injury if detected early. Renal damage can be due to several different mechanisms affecting different segments of the nephron, renal microvasculature or interstitium. Clinical signs may not be apparent in the early stages and assessment of renal function should include thorough evaluation of glomerular filtration rate, proximal and distal tubular function. A kidney biopsy may be indicated to establish the cause and effect relationship. The presence of comorbid conditions such as older age, diabetes mellitus, hypertension and congestive heart failure have a significant influence on the patient's ability to recover from the toxic effects. A significant degree of drug-induced renal toxicity is only acceptable if the causative agent is used for the curative treatment of an underlying disease but not if the aim is the palliative or supportive therapy. The decision to reduce the dose or to stop the toxic agent must be based on the ultimate goal of therapy and the patient's baseline health status.

Antifungal Agents↗

PubMedDate not supplied

Expression of NHERF-1, NHERF-2, PDGFR-alpha, and PDGFR-beta in normal human kidneys and in renal transplant rejection.

Sodium-hydrogen exchanger regulatory factor-1 and -2 (NHERF-1 and NHERF-2) are adaptor proteins that regulate renal electrolyte transport and interact with the platelet-derived growth factor receptors (PDGFR). The distribution of the NHERF proteins and PDGFR was studied in normal human kidneys and in renal transplant rejection using immunocytochemistry. In normal kidneys, NHERF-1 was detected in proximal tubules. NHERF-2 was detected in glomeruli, peritubular capillaries, and collecting duct principal cells. NHERF-2 was also weakly detected in the proximal tubule. PDGFR-beta was detected in glomeruli but not in tubules while PDGFR-alpha was detected in renal tubules and minimally in glomeruli. Acute and chronic transplant rejection was associated with increased expression of PDGFR-alpha in tubules and expression in the glomeruli. PDGFR-beta expression in the glomeruli was increased in transplant rejection and became detectable in tubules. Expression of NHERF-1 and NHERF-2 was not different in the patient groups. These results indicate that in contrast to the rat, both NHERF isoforms are detected in the human proximal tubule. In renal transplant rejection, there is increased expression of both PDGFR subtypes consistent with a role for PDGF in injury or repair.

Acute Disease↗