Double Whammy: Pigment Nephropathy and Warfarin-related Nephropathy As Aetiology for Acute Kidney Injury in a Patient With Mechanical Heart Valves

It is well known that patients with mechanical heart valves may develop sheer stress related hemolysis and consequent pigment related nephropathy. Warfarin Related Nephropathy (WRN) is a relatively new entity and defined as Acute Kidney Injury (AKI) in the setting of an INR of > 3.0 excluding other obvious etiologies. A biopsy diagnosis of WRN is conducted when red blood cell casts are noted filling and blocking the tubules; additionally, glomerular hemorrhage may be observed. We describe a patient with mechanical heart valves on oral anticoagulation who developed both pigment nephropathy and WRN causing AKI.

Pigment Nephropathy: Novel Insights into Inflammasome-Mediated Pathogenesis

Pigment nephropathy is an acute decline in renal function following the deposition of endogenous haem-containing proteins in the kidneys. Haem pigments such as myoglobin and haemoglobin are filtered by glomeruli and absorbed by the proximal tubules. They cause renal vasoconstriction, tubular obstruction, increased oxidative stress and inflammation. Haem is associated with inflammation in sterile and infectious conditions, contributing to the pathogenesis of many disorders such as rhabdomyolysis and haemolytic diseases. In fact, haem appears to be a signalling molecule that is able to activate the inflammasome pathway. Recent studies highlight a pathogenic function for haem in triggering inflammatory responses through the activation of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome. Among the inflammasome multiprotein complexes, the NLRP3 inflammasome has been the most widely characterized as a trigger of inflammatory caspases and the maturation of interleukin-18 and -1β. In the present review, we discuss the latest evidence on the importance of inflammasome-mediated inflammation in pigment nephropathy. Finally, we highlight the potential role of inflammasome inhibitors in the prophylaxis and treatment of pigment nephropathy.

Pigment Nephropathy: Novel Insights into Inflammasome-Mediated Pathogenesis

Pigment nephropathy is an acute decline in renal function following the deposition of endogenous haem-containing proteins in the kidneys. Haem pigments such as myoglobin and haemoglobin are filtered by glomeruli and absorbed by the proximal tubules. They cause renal vasoconstriction, tubular obstruction, increased oxidative stress and inflammation. Haem is associated with inflammation in sterile and infectious conditions, contributing to the pathogenesis of many disorders such as rhabdomyolysis and haemolytic diseases. In fact, haem appears to be a signaling molecule that is able to activate the inflammasome pathway. Recent studies highlight a pathogenic function for haem in triggering inflammatory responses through the activation of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome. Among the inflammasome multiprotein complexes, the NLRP3 inflammasome has been the most widely characterized as a trigger of inflammatory caspases and the maturation of interleukin-18 and -1β. In the present review, we discuss the latest evidence on the importance of inflammasome-mediated inflammation in pigment nephropathy. Finally, we highlight the potential role of inflammasome inhibitors in the prophylaxis and treatment of pigment nephropathy.

Heme-pigment nephropathy after transurethral resection of prostate cancer

Introduction: Transurethral resection of the prostate is one of the most common surgical procedures performed in men to relieve bladder outlet obstruction, most often due to benign prostatic hyperplasia. However, transurethral resection of the prostate may also be used in patients with metastatic prostate cancer who have bladder outlet obstruction. Acute kidney injury after transurethral resection of the prostate has been described and attributed to a variety of mechanisms, including acute tubular necrosis, rhabdomyolysis, and hemolysis with heme-pigment nephropathy. However, to our knowledge, no case of kidney biopsy-proven heme-pigment nephropathy due to hemolysis from a transurethral resection of the prostate procedure has been published to date. Case description: We describe a case of an 82-year-old man with metastatic prostate cancer who presented with severe oliguric renal failure 2 weeks after transurethral resection of the prostate for bladder outlet obstruction. Laboratory studies showed evidence of hemolysis, and a kidney biopsy showed heme-pigment cast nephropathy. Conclusions: We hypothesize that the patient’s kidney injury was induced by hemolysis resulting from rapid absorption of hypotonic fluid administered during the transurethral resection of the prostate procedure. Patients with prostate cancer undergoing transurethral resection of the prostate for bladder outlet obstruction may experience severe complications related to rapid absorption of hypotonic fluid. Our case illustrates the importance of nephrology evaluation and kidney biopsy in patients with benign and malignant prostate conditions who experience post-transurethral resection of the prostate syndrome and acute kidney injury in order to better characterize these complications, and to develop preventative strategies for future cases.