Acute Kidney Injury in Obstetric Patients.

Obstetric-related acute kidney injury (obstetric AKI) is an important and complex public health problem; its early recognition and proper treatment are key in preventing maternal and fetal adverse outcomes. While the incidence of obstetric AKI has drastically declined in some developing countries due to reduction of sepsis-related causes, the opposite has been observed in other developed nations in the last decade due to advanced maternal age and the presence of comorbidities. The diagnosis of obstetric AKI has been made difficult by the physiologic decrease in serum creatinine of pregnancy as well as the absence of a uniform definition for AKI in this population. The most common causes of obstetric AKI include pre-renal etiologies such as hyperemesis gravidarum and post-abortal sepsis, intra-renal causes which comprise the thrombotic microangiopathies (preeclampsia/HELLP, thrombotic thrombocytopenic purpura, pregnancy associated-hemolytic uremic syndrome, lupus nephritis), and post-renal causes due to obstruction from kidney stones or iatrogenic injuries during delivery. A kidney biopsy is rarely required and should be reserved for cases where the diagnosis will change management, preferably before the third trimester. A multidisciplinary approach with the maternal-fetal-medicine specialist and nephrologist, along with the intensivist and hematologist may be needed. In this review, we will present the latest updates on the global epidemiology, focus on the most challenging thrombotic microangiopathy diagnoses, summarize treatment recommendations, and delineate the ongoing challenges as well as novel strategies to tackle this public health burden which does not seem to be disappearing.

Proliferative glomerulonephritis with monoclonal immunoglobulin deposits associated with parvovirus B19.

Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is included in the group of dysproteinaemias causing renal disease. Only a minority of cases are associated with a haematological malignancy. Two cases have been linked to acute parvovirus B19 infections. We report a 36-year-old African-American woman who presented with renal dysfunction, proteinuria, haematuria and a kidney biopsy reported as PGNMID with IgG3-kappa deposits. Her evaluation for a haematological malignancy was unrevealing. Her parvovirus IgM and IgG levels were positive. The patient was initially treated with an ACE inhibitor and spontaneously remitted with minimal proteinuria after 1 month. Repeat parvovirus B19 serologies 6 months later showed persistent IgG and DNA by PCR positivity but IgM negativity. Given the clinical scenario, we believe that her PGNMID was induced by acute parvovirus B19 infection, which appeared to resolve once her acute infection abated. In this report, we describe our latest understanding of PGNMID.

Light chain proximal tubulopathy with cast nephropathy in monoclonal gammopathy of renal significance.

Kidney tubular disorders due to monoclonal immunoglobulin light chains are common manifestations of B-cell neoplasm. Cast nephropathy (CN) is the most frequent type of these disorders and may present with acute kidney injury (AKI) due to the presence of excess light chains in the distal tubules. Light chain proximal tubulopathy (LCPT) is an uncommon form of renal disease and may present as Fanconi syndrome due to proximal tubular cell damage by intracellular deposition of light chains. The concomitant disorder of both CN and LCPT is rare given the inherent differences in the biochemical properties of the immunoglobulin light chains of each disorder. We report a 64-year-old man who presented with AKI and Fanconi syndrome who was discovered to have both CN and LCPT due to the underlying disorder of monoclonal gammopathy of renal significance and who has responded favourably with conventional chemotherapy. We also review the existing literature on this interesting subject.