Case Reports in Nephrology

Assessing transplant suitability can be a meticulous process, involving multiple investigations and various specialties. This process is well described in the latest KDIGO guidelines. We recently asked ourselves if those guidelines are still relevant to current clinical practice given the rapid evolution of modern medicine, especially in the field of oncology. We present the complicated case of a 60-year-old woman with ESKD (end-stage kidney disease) and a prior history of cancer, with secondary urological complications, to illustrate different interesting considerations for KT (kidney transplant). Our patient was diagnosed with rectal cancer at the age of 46, for which she was treated with surgery and radiotherapy before developing chronic radiation cystitis. This was followed by repeated urinary tract infections and secondary nephrolithiasis, ultimately leading to severe bilateral hydronephrosis and obstructive ESKD. We know that the type of cancer and its characteristics should be evaluated in detail, and we should offer patient-tailored recommendations after a multidisciplinary evaluation. In our case, the prior rectal cancer is not to be feared because curative treatment has been achieved and the patient has been cancer-free for 14 years, knowing that this type of cancer is not at high risk of recurrence after transplantation. The frail urological anatomy, however, represents a bigger challenge. Not only does it complicate the technical feasibility of KT but it also increases the risk of complications and graft failure. It is difficult to clearly determine KT possibility when considering it in such patients. What is clear on the other hand is that such a decision should be taken considering the choice of the patient and the involved physicians. We should also consider the potential benefits and risks of KT in order to make an informed decision.

Hypercalcemia is a common and potentially serious electrolyte abnormality that is often observed in patients with chronic kidney disease (CKD). When malignancy is considered, parathyroid hormone-related protein (PTHrP) levels are often measured. PTHrP is produced by cancer cells and mimics the effects of parathyroid hormone (PTH) to elevate serum calcium concentrations. The amino and carboxy termini of PTHrP are of functional relevance. C-terminal PTHrP levels accumulate with CKD and can be elevated in normocalcemic CKD patients who lack malignancy. The existence of amino (N)-terminal and carboxy (C)-terminal PTHrP assays and how their concentrations are impacted by CKD are reviewed herein. The case of a patient on maintenance hemodialysis who developed prolonged hypercalcemia with elevated PTHrP concentrations is presented. The workup revealed suppressed intact PTH, low 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D levels. The initial PTHrP assay returned elevated. However, it was unappreciated that it was the C-terminal assay and the patient underwent an unnecessary search for malignancy. A subsequent N-terminal PTHrP assay returned within the normal range. Many commercial labs run the C-terminal PTHrP assay as their first-line test. This can lead to inaccurate differential diagnoses in hypercalcemic patients with CKD. We emphasize the need to specifically request N-terminal PTHrP assays in patients with advanced kidney disease when humoral hypercalcemia of malignancy is suspected.

While ureteropelvic junction (UPJ) obstruction is a well-recognized cause of unilateral or bilateral upper urinary tract dilatation in infants and the pediatric population, its occurrence in adults is less recognized. We present the case of a 68-year-old man who was being evaluated for chronic orthostatic hypotension and was incidentally found to have asymptomatic microscopic hematuria on urinalysis. A CT scan of the abdomen/pelvis, without and with contrast, revealed severe bilateral hydronephrosis due to UPJ obstruction. The patient has remained asymptomatic with preserved normal renal function over 7 years of follow-up.

A middle-aged immigrant male from a region with endemic tuberculosis who had a history of end-stage kidney disease presented to the emergency room for routine hemodialysis and abdominal swelling. He was admitted to the medicine service for suggested daily dialysis to improve his volume overload, which was attributed to nephrogenic ascites. He was found to have several findings concerning for systemic illness, including fevers, night sweats, hypercalcemia, lymphadenopathy, omental thickening, ascitic fluid with a serum ascites albumin gradient of less than 1.1 gm/dL, and exudative pleural effusions. Our suspicion for hematologic malignancy versus disseminated infection was high. During admission, there were many diagnostic challenges in obtaining histologic and bacteriologic confirmation of our leading suspected diagnosis, disseminated tuberculosis. Ultimately, tuberculosis infection was confirmed with histologic evidence of granulomatous inflammation of cervical lymph node and sputum culture positive for Mycobacterium tuberculosis. This case highlights the necessity for every patient presenting with new ascites to undergo diagnostic paracentesis. Nephrogenic ascites is a rare syndrome that is possible in volume overloaded states but is a diagnosis of exclusion that should be supported by an exudative serum ascites albumin gradient and no evidence of an alternate etiology.

We experienced a case of myeloperoxidase antineutrophil cytoplasmic antibody (MPO-ANCA)-associated vasculitis after Moderna COVID-19 vaccination. An 82-year-old woman developed pyrexia and general malaise one month after her third booster vaccine, and the symptoms persisted. Blood testing revealed inflammation, a high level of MPO-ANCA, and microscopic hematuria. MPO-ANCA-associated vasculitis was diagnosed by renal biopsy. The symptoms improved with steroid therapy. Common adverse reactions to mRNA vaccines against COVID-19 include pyrexia and general malaise, but MPO-ANCA-associated vasculitis can also occur. If pyrexia, prolonged general malaise, urinary occult blood, or renal impairment is observed, the onset of MPO-ANCA-associated vasculitis should be considered.

Antitubular basement membrane (anti-TBM) antibody disease is an extremely rare disorder. It may be idiopathic or secondary to exposure of the proximal tubular basement membrane, triggered by tubular injury due to acute pyelonephritis, acute allergic interstitial nephritis, or kidney allograft rejection. The histopathology of anti-TBM antibody disease is characterized by strong linear deposits of IgG with complement C3 along the proximal tubular cell basement membranes. The staining is restricted to proximal tubules. Currently, a kidney biopsy with these pathognomonic findings is the only diagnostic method. Serological testing and titers for anti-TBM antibodies are not clinically standardized. Our patient had pyelonephritis and possibly acute allergic interstitial nephritis as a result of nivolumab infusion. The kidney biopsy demonstrated dense interstitial infiltrates of neutrophil-rich interstitial inflammation, neutrophilic casts, and neutrophilic tubulitis consistent with acute pyelonephritis, as well as areas of mixed inflammation with lymphocytic tubulitis suggesting concurrent acute interstitial nephritis. The presence of linear IgG staining along proximal but not distal tubular basement membranes was diagnostic of anti-TBM antibody disease, favored to be due to both triggers. The patient was treated with discontinuation of nivolumab, intravenous antibiotics, and corticosteroids and was supported with hemodialysis. After 6 weeks, the patient’s kidney function recovered enough to discontinue hemodialysis and had significant renal improvement.