Reversal Of Acute Renal Failure Research Articles

Postoperative nutritional support of the patient with gut gangrene\u2014a case report

BackgroundBowel necrosis is a commonly observed condition in elderly patients with longstanding diabetes. In such condition, intestinal resection is usually performed for the removal of the gangrenous part. Post-surgical dietary management after bowel resection poses several challenges for the health care team.Case presentationThe case presented in this study is that of an elderly diabetic male who developed acute renal failure as a result of neglect in post-surgical feeding after intestinal resection. After the intervention by a trained dietitian, a transitional diet was planned and successfully executed, resulting in reversal of acute renal failure, dehydration, and post-surgical stress. Several complications including hepatic dysfunction and mouth ulcers were resolved through well-planned transitional diet. The patient was finally discharged in a stable health condition and was regularly followed up for any nutritional or medical issues.ConclusionNeglects in nutritional care of patients can have severe implications including development of medical complications, resulting in increased length of hospital stay, augmenting the disease stress of the patient and family, and finally the preventable drainage of several human and monetary resources. Therefore, recognition of nutritional intervention as an important part of in-hospital health care may have social as well as economic impacts.

Reversal of acute renal failure by bortezomib-based chemotherapy in patients with multiple myeloma

Paraprotein induced renal failure is a frequent complication of multiple myeloma and is associated with poor survival. Previously, reversal of renal function has been hampered by the lack of fast acting and highly effective myeloma therapy and most patients remained or became dependent on hemodialysis. Here we show reversal of acute paraprotein-induced renal failure by bortezomib-based therapy in 5 out of 8 patients. Improvement of renal function was preceded by a significant reduction in paraprotein concentration in all patients, with improvement in renal function.

Relapse of HIV-associated nephropathy after discontinuing highly active antiretroviral therapy

F.H., a 53-year-old African American woman presented to her primary care provider with acute renal failure (creatinine 2.7 mg/dl from baseline of 1.3 mg/dl) and proteinuria (1.6 g of protein per 24 h). Her past medical history was significant only for hypertension and asthma. Evaluation revealed a positive HIV antibody and a CD4 cell count of 281 cells/μl. F.H. was started on antiretroviral therapy with zidovudine, and a renal biopsy demonstrated glomerular capillary loop collapse and a tubulointerstitial lymphocyte infiltrate with cystically dilated tubules and atrophy consistent with HIV-associated nephropathy (HIVAN). In addition to her antiretroviral therapy she was treated with an angiotensin-converting enzyme inhibitor and a course of corticosteroids. Her creatinine level peaked at 4.6 mg/dl and proteinuria was at approximately 3 g per 24 h. Over the next 3 years her creatinine and proteinuria levels stabilized as she was treated with zidovudine and lamivudine with a relatively suppressed viral load and rising CD4 cell count (see Fig. 1). In March 1999, she was started on HAART with stavudine, didanosine and efavirenz resulting in complete viral suppression and a rise in the CD4 cell count to approximately 900 copies/μl for 2 years. During this period the creatinine level declined to 1.8 mg/dl and urinary protein dropped to 500 mg per 24 h. In August 2001, F.H. discontinued HAART as a result of the side effects of therapy. Her viral load quickly rose to over 300 000 copies/ml and her renal function worsened, with a creatinine level of 3.8 mg/dl in May 2002. A renal ultrasound revealed small echogenic kidneys, consistent with chronic disease, and renal biopsy confirmed recurrent active HIVAN. F.H. was again treated with corticosteroids and HAART, now consisting of zidovudine/lamivudine/abacavir and efavirenz. Over the next 3 years her viral load was fully suppressed on this regimen and her renal function, although severely compromised, has stabilized (estimated glomerular filtration rate 15 ml/min per 1.73 m2) avoiding the need for renal replacement therapy. In addition, there was a dramatic decline in proteinuria from an estimated 5 g to 1 g per 24 h.Fig. 1: Serum creatinine (mg/dl) and urine protein to creatinine ratio (grams protein/grams creatinine) versus time, during therapy with HAART. The upper bars indicate the antiretroviral treatment regimen during the corresponding time intervals. The fluctuation in HIV viral load in relation to time and treatment is indicated in the upper graph. CD4 cell count (cells/ml) at various points in time is indicated numerically below the treatment bars. The lower graph indicates serum creatinine (▵) and urine protein to creatinine ratios (□) versus time and in relation to the ongoing treatment indicated in the upper treatment bars. ABC, Abacavir; ddI, didanosine; D4T, stavudine; EFV, efavirenz; 3TC, lamivudine; ZDV, zidovudine.Epidemiological studies have shown a correlation between increasing HIV viral load, decreasing CD4 cell count and the occurrence of proteinuria and renal failure [1], as well as a reduction in the incidence of HIVAN in patients treated with HAART [2]. Previous case reports have demonstrated a reversal of acute renal failure and histological changes on biopsy after short courses of antiretroviral therapy [3]. Several observational cohort studies have demonstrated a decreased need for renal replacement therapy for patients treated with antiretroviral therapy compared with those not so treated [4–6]. This case supports the hypothesis that HIVAN can be treated by the suppression of viral replication with HAART, and when initiated early may remove the need for renal replacement therapy and provide long-term stabilization of disease. Unlike the previous reported cases, this case suggests a risk of relapse of disease after discontinuing HAART. This suggests that a history of HIVAN alone may be an indication for indefinite HAART, even with an adequate CD4 cell count and despite mild to moderate side effects.

Arginine-Vasopressin in severe septic vs. non-septic shock in extremely low birth weight infants with acute renal failure

Background: Recent clinical investigations have demonstrated that arginine-vasopressin (AVP) may be a valuable alternative or adjunct to common pressor agents in various forms of shock (1, 2). Although, typically septic shock is characterized by AVP deficiency and pressor hypersensitivity to the exogenous hormone, AVP has also been successfully employed in other shock forms that are usually not characterised by AVP deficiency. Aim: To assess the efficacy of AVP as a pressor adjunct to norepinephrine and epinephrine in severe septic vs. non-septic shock in extremely low birth weight infants (ELBW) with acute renal failure (urine output: <0.5ml/kg/h). Patients and Methods: Assessment of AVP therapy as a rescue therapy in three ELBW infants (mean birth weight: 600±30 grams) with severe septic shock and acute renal failure and three ELBW infants (mean birth weight: 770±110grams) with severe non-septic shock and acute renal failure. Main outcome measure was restoration of mean arterial blood pressure (MAP) with reversal of acute renal failure, and survival at discharge. Results: In the group with severe septic shock two hours after starting AVP (dosage:0.04–0.4 U/kg/h) a rise in MAP from 31.7±9.5 to 39.7±19.1mmHg was seen; urine output increased to 9.7±11.5ml/h, and a slight decrease in serum lactate from 9.6±6.7 mmol/l to 8.9±6.2 was noticed. In the group with severe non-septic shock, MAP increased from 25±5 to 38.7±8.3mmHg within 2h of AVP medication (dosage: 0.04–0.4U/kg/h); urine output increased to 5.4±3.2ml/h. Serum lactate moderately increased from 14.3±5.1 to 15.2±6.2 mmol/l. In the non-septic group cardiac and renal changes were only transient and did not impact on the poor prognosis. Mortality rate was 1/3 in the sepsis group vs. 3/3 in the non-septic group. Conclusion: This is the first report on AVP in severe hypotensive shock in ELBW infants. AVP appears to be effective in restoring MAP and subsequent reversal of acute renal failure. Maintenance of adequate and sustained tissue perfusion appears to be dependent on the underlying cause of hypotension. Although AVP seems to be an effective rescue therapy in severe septic shock in ELBW infants further evaluation in controlled clinical trials is warranted.

Mechanisms of Renal Cell Repair and Regeneration after Acute Renal Failure

In many cases, acute renal failure (ARF) is the result of proximal tubular cell injury and death and can arise in a variety of clinical situations, especially following renal ischemia and drug or toxicant exposure. Although much research has focused on the cellular events leading to ARF, less emphasis has been placed on the mechanisms of renal cell repair and regeneration, although ARF is reversed in over half of those who acquire it. Studies using in vivo and in vitro models have demonstrated the importance of proliferation, migration, and repair of physiological functions of injured renal proximal tubular cells (RPTC) in the reversal of ARF. Growth factors have been shown to produce migration and proliferation of injured RPTC, although the specific mechanisms through which growth factors promote renal regeneration in vivo are unclear. Recently, interactions between integrins and extracellular matrix proteins such as collagen IV were shown to promote the repair of physiological functions in injured RPTC. Specifically, collagen IV synthesis and deposition following cellular injury restored integrin polarity and promoted repair of mitochondrial function and active Na(+) transport. Furthermore, exogenous collagen IV, but not collagen I, fibronectin, or laminin, promoted the repair of physiological functions without stimulating proliferation. These findings suggest the importance of establishing and/or maintaining collagen IV-integrin interactions in the stimulation of repair of physiological functions following sublethal cellular injury. Furthermore, the pathway that stimulates repair is distinct from that of proliferation and migration and may be a viable target for pharmacological intervention.

Acute renal failure secondary to solid tumor renal metastases: Cases report and review of the literature

Renal metastases from solid tumors to both kidneys rarely result in acute renal failure (ARF). We present a case of squamous cell pulmonary carcinoma responsible for ARF due to (1) extensive (50% to 75%) bilateral parenchymal infiltration and replacement accompanied by tissue destruction, (2) widespread vascular invasion and thrombosis resulting in ischemia, and (3) histological evidence for foci of distal intratubular obstruction and pyelonephritis. Five additional cases, including one pulmonary cancer, causing ARF from extensive tissue replacement and destruction are reviewed. In a separate case, ARF resulted from lymphatic metastases rather than from parenchymal destruction or obstruction. Common findings in all six reported cases include bilaterally enlarged kidneys and progressive oligoanuria despite correction of prerenal or postrenal conditions. In our patient and in one other prior reported case, extrarenal obstruction was not considered important because invasive therapeutic procedures were unsuccessful in reversing ARF. In one case, irradiation of kidney tumor resulted in reversal of ARF. These cases emphasize the rare potential for solid tumors to metastasize to both kidneys and result in irreversible oligoanuric ARF. A high level of suspicion is required, and an early diagnosis may result in reversible ARF if the tumor is amenable to chemotherapy or irradiation.

Reversal of acute renal failure by kidney revascularisation

To assess whether acute renal failure, due to total or subtotal renal artery occlusion, can be reversed by kidney revascularisation. A retrospective review of surgery for kidney salvage in anuric patients at a University Hospital. From 1983 to 1993, eight patients were operated on for occlusive renal artery disease as a cause of acute renal failure, requiring preoperative haemodialysis. On admission the mean serum creatinine was 40 mg/l (354 mumol/dl). The oligoanuria lasted from 12 h to 3 weeks. Renal length of 8 cm or more and visualisation of a patent distal renal artery branches on aortography were arguments that return of renal function could be expected after revascularisation of these non-functioning kidneys. Revascularisation restored immediate urine flow in six cases, with no further need for dialysis in four. Two patients remained oliguric despite successful reperfusion. One of them could be weaned from dialysis after 1 month. Two patients died postoperatively. Five of the eight patients left the hospital with restored renal function. Patients with acute renal function deterioration due to ischemia of a single or both kidneys can benefit from prompt revascularisation, with significant recovery of renal function in most of them.

Acute Renal Allograft Dysfunction in the Setting of Deep Venous Thrombosis: A Case of Successful Urokinase Thrombolysis and a Review of the Literature

Acute renal allograft vein thrombosis is a rare but serious complication of renal transplantation. When occurring in the early posttransplant period it is usually associated with surgical complications and often results in the loss of the graft. At later stages, when graft function has stabilized, its development may then be associated with underlying disorders such as glomerulonephritis, immunosuppressive therapy, increased hematocrit, acute rejection, or extension of lower extremity venous thromboses. We report a case of acute allograft dysfunction occurring in the setting of extensive deep vein thrombosis. In our patient, thrombosis in the setting of acute graft tenderness and swelling, anuria, and an increasing creatinine strongly suggest a diagnosis of acute allograft renal vein thrombosis. We describe a successful reversal of acute renal failure through urokinase thrombolysis and review the current literature on the use of thrombolytic agents for the treatment of acute renal allograft vein thrombosis.

Reversal of acute renal failure following percutaneous transluminal recanalization of an atherosclerotic renal artery occlusion

Thrombosis of the renal artery to a single functioning kidney is a known cause of anuric acute renal failure in atherosclerotic hypertensive patients. In the present report, recovery of renal function rapidly occurred following transluminal recanalization of the occluded artery with a 7F catheter after a 5-week period of anuria. The most interesting feature was that improvement of renal artery permeability was observed following a minimal interventional procedure.

Reversal of acute renal failure using hemodilution with hydroxyethyl starch.

Acute renal failure (ARF) was induced in two groups of unilaterally nephrectomized dogs by occluding the renal artery, vein, and ureter of the remaining kidney for 2 hours. The control group (Group I), had no therapy; in the experimental group (Group II), isovolemic hemodilution was carried out using 6% hydroxy ethyl starch (HES) as diluent. The hematocrit in the experimental animals was lowered from 41.62 +/- 3.6% to 23.75 +/- 5.2% after renal occlusion. The mean arterial pressure and the mean pulmonary arterial pressure were unchanged in either group. Cardiac output increased following hemodilution from 1.66 +/- 0.35 to 2.70 +/- 0.50 L/min while it remained unchanged in Group I. Control animals developed ARF characterized by progressive rise in serum creatinine concentration and death. Only 1/7 Group I animals was alive on day 7 compared to 7/7 of Group II (p less than 0.01). ARF that developed initially in Group II began to resolve after day 4. There was a progressive and significant fall in serum creatinine concentration from 6.48 +/- 0.67 mg/dl on day 4 to 4.08 +/- 0.83 mg/dl on day 7 (p less than 0.001). Immediate isovolemic hemodilution with HES can reverse ARF induced by ischemia.