Clinical profile and outcome of pigment-induced nephropathy

Abstract

BackgroundPigment nephropathy represents one of the most severe complications of rhabdomyolysis or hemolysis.MethodsWe performed a retrospective observational study to analyze the etiology, clinical manifestation, laboratory profile and outcome in patients with biopsy-proven pigment-induced nephropathy between January 2011 and December 2016. History, clinical examination findings, laboratory investigations and outcome were recorded.ResultsA total of 46 patients were included with mean follow-up of 14 ± 5.5 months. Mean age was 40.15 ± 12.3 years, 65% were males (male:female, 1.8:1) and ∼37 (80.4%) had oliguria. Mean serum creatinine at presentation and peak creatinine were 7.5 ± 2.2 and 12.1 ± 4.3 mg/dL, respectively. Evidence of rhabdomyolysis was noted in 26 patients (64%) and hemolysis in 20 patients (36%). Etiology of rhabdomyolysis include snake envenomation (10 patients), seizures (7), strenuous exercise (5), wasp sting (2) and rifampicin induced (2). The causes of hemolysis include rifampicin induced (7 patients), sepsis (5), malaria (3), mismatched blood transfusion/transfusion reaction (3) and paroxysmal nocturnal hemoglobinuria (2). On renal biopsy, two patients had acute interstitial nephritis and two had immunoglobulin A deposits in addition to pigment nephropathy. All except one (97.8%) required hemodialysis (HD) during hospital stay and mean number of HD sessions was 9 ± 2. A total of three patients with sepsis/disseminated intravascular coagulation died, all had associated hemolysis. On statistical analysis, there was no difference between AKI due to rhabdomyolysis and hemolysis except for high creatine phosphokinase in patients with rhabdomyolysis and Lactate dehydrogenase level in patients with hemolysis. At mean follow-up, five patients (12%) progressed to chronic kidney disease (CKD).ConclusionsPigment nephropathy due to rhabdomyolysis and hemolysis is an important cause of renal failure requiring HD. The prognosis was relatively good and depends on the etiology; however, long-term studies and follow-up are needed to assess the true incidence of CKD due to pigment nephropathy.

Plasma exchange for heparin‐induced thrombocytopenia in patients on extracorporeal circuits: A challenging case and a survey of the field

“…The utilization of TPE in reducing plasma cell free‐hemoglobin and managing renal injury has been previously described However, the current ASFA 2016 guidelines do not include the reduction of cell free hemoglobin as an indication for TPE and hemodialysis remains the main stay therapy for management of AKI secondary to pigment nephropathy . Our patient developed AKI in the setting of active intravascular hemolysis, which required hemodialysis during his postoperative recovery.…”

“…The utilization of TPE in reducing plasma cell freehemoglobin and managing renal injury has been previously described 35,36 However, the current ASFA 2016 guidelines do not include the reduction of cell free hemoglobin as an indication for TPE and hemodialysis remains the main stay therapy for management of AKI secondary to pigment nephropathy. 21,37,38 Our patient developed AKI in the setting of active intravascular hemolysis, which required hemodialysis during his postoperative recovery. It is difficult to assess the individual contributions of poor renal perfusion, including factors such as recent prior AKI and elevated cellfree hemoglobin (Table 1, Figure 3B) leading to the development of AKI postoperatively in our patient.…”

Acute Kidney Injury due to Anticoagulant-Related Nephropathy : A Suggestion for Therapy

“…Generally, glomerular macrohematuria is considered a marker of glomerular basement membrane damage and inflammation [5] but, it can be also associated to AKI [6]; in fact, haematuria results in tubular injury in pigment-induced nephropathy (PIN), IgA nephropathy (IgAN), thin basement membrane nephropathy, and ARN [6,7]. In vitro tubular cytotoxicity after RBC administration encouraged reevaluation of the predominant role of tubular obstruction in haematuria-associated renal damage.…”

“…ARN and PIN share some pathogenetic features. Few evidence [7,13] suggest that mannitol together with bicarbonate have no advantage over fluid resuscitation in managing AKI due to rhabdomyolysis, and its use remains controversial. However, randomized controlled trials are lacking, and its beneficial effect cannot be excluded [14].…”

Rosuvastatin-related rhabdomyolysis causing severe proximal paraparesis and acute kidney injury

“…In severe cases of rhabdomyolysis, once AKI is established, it requires close monitoring as a significant proportion of these cases may require renal replacement therapy. These patients may progress to developing a residual renal damage and CKD 18 19…”