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Acute Phosphate Nephropathy with Diffuse Tubular Injury Despite Limited Calcium Phosphate Deposition

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Acute Phosphate Nephropathy with Diffuse Tubular Injury Despite Limited Calcium Phosphate Deposition □ CASE REPORT □ Acute Phosphate Nephropathy with Diffuse Tubular Injury Despite Limited Calcium Phosphate Deposition Yosuke Yamada 1, Makoto Harada 1, Akinori Yamaguchi 1, Mai Sugiyama 1,TaroKanno1, Koji Hashimoto 1, Takashi Ehara 2, Hisashi Shimojo 3, Hidekazu Shigematsu 3 and Yuji Kamijo 1 Abstract An 86-year-old woman developed acute kidney injury after colonoscopy. A renal biopsy showed diffuse tu- bular injury with minimal calcium phosphate deposits (CPDs), which were thought to be caused by an oral sodium phosphate bowel purgative before colonoscopy. According to these findings, she was diagnosed with acute phosphate nephropathy (APhN). In contrast to previous reports of diffuse tubular injury associated with tubular CPDs in APhN, this case demonstrated diffuse tubular injury despite a limited distribution of CPDs, suggesting that calcium phosphate can cause tubular injury without deposition. This case thus supports the hypothesis that urinary calcium phosphate crystals may cause tubular injury via other mechanisms, including inflammatory cytokines. Key words: acute phosphate nephropathy, oral sodium phosphate, colonoscopy, acute and reversible kidney injury, calcium phosphate crystal, drug-induced acute kidney injury (Intern Med 55: 2229-2235, 2016) (DOI: 10.2169/internalmedicine.55.5864) CPD-induced luminal obstruction and inflammation, fol- Introduction lowed by tubulointerstitial injury. We herein report a patient with APhN who showed diffuse tubular injury despite the Acute kidney injury (AKI) can be induced by various limited presence of CPDs. This case thus suggests that high drugs, including nonsteroidal anti-inflammatory drugs concentrations of calcium phosphate in the urine may result (NSAIDs), antibiotics, cisplatin, and contrast media. Oral in direct injury of the tubular epithelial cells, even in the ab- sodium phosphate (OSP) is used as a bowel purgative before sence of CPDs. colonoscopy and has also been shown to result in AKI, though this cause is not widely recognized. Desmeules et al. Case Report first described acute phosphate nephropathy (APhN) as a novel cause of drug-induced AKI in 2003 (1). Risk factors An 86-year-old woman underwent a routine colonoscopy for APhN include older age, female sex, hypertension, dia- checkup at a local hospital. She took 50 OSP tablets (50 g) betes mellitus, chronic kidney disease (CKD), and treatment as a bowel purgative prior to the examination. She became with angiotensin-converting enzyme inhibitors, angiotensin aware of general fatigue and oliguria shortly after the ex- receptor blockers (ARBs), NSAIDs, and diuretics (Table 1). amination and visited the hospital 6 days after colonoscopy. However, there have been few detailed pathological studies At that time, a physical examination showed mild edema of of APhN. Markowitz et al. described the detailed pathologi- the face and legs and laboratory data showed severe kidney cal findings of APhN in 21 patients (2) (Table 2-4). Accord- dysfunction (serum creatinine, 5.3 mg/dL; blood urea nitro- ing to representative pathological findings of diffuse and gen, 82 mg/dL). No obvious signs of dehydration were de- abundant calcium phosphate deposits (CPDs) in the kidney tected by physical or laboratory examinations (fractional ex- tubule lumens, APhN is thought to develop as a result of cretion of sodium, 3.5%) (Table 5, 6). She was admitted to １Department of Nephrology, Shinshu University School of Medicine, Japan, ２Department of Health and Sport Science, Matsumoto University Graduate School of Medicine, Japan and ３Department of Pathology, Shinshu University School of Medicine, Japan Received for publication May 29, 2015; Accepted for publication December 15, 2015 Correspondence to Dr. Yuji Kamijo, [email protected] 2229 Intern Med 55: 2229-2235, 2016 DOI: 10.2169/internalmedicine.55.5864 Table 1. Risk Factors for Acute Phosphate Nephropa- basement membrane, and flattening of tubular epithelial thy. cells were detected (Fig. 2). The interstitial area was found Risk factor Reference to have increased and it occupied 51% of the total cortical Chronic kidney disease [12] area, with tubular atrophy, interstitial edema, and fibrosis. RABs (ACE-Is and ARBs) [13] Tubular basophilic deposits accompanied by tubular epithe- Advanced age [12] [14] lial cell injury were also detected in several tubules (Fig. 3). Drugs (diuretics, NSAIDs) [12] [15] Female sex [16] These deposits were positive for von Kossa stain, indicating Comorbidity (hypertension, diabetes) [12] [14] that they were CPDs (Fig. 4A). These CPDs were located in ACE-I: angiotensin-converting enzyme inhibitor, ARB: angiotensin the distal tubules, rather than the proximal tubules, and were receptor blocker, NSAID: nonsteroidal anti-inflammatory drug, RAB: renin-angiotensin blocker distributed focally, only occurring in 2% of tubular lumens (19/673), whereas damaged tubules with tubular vacuolation and dilation and detachment and flattening of tubular epithe- the hospital and administered intravenous fluids for 3 days, lial cells occurred diffusely in 53% (357/673) of tubular lu- however, her serum creatinine levels remained elevated (5.02 mens (Fig. 4B). Arterial lesions, including fibrous intimal mg/dL). Ten days after colonoscopy, she was transferred to thickening and hyaline changes, were scarce in the kidney our hospital for detailed examinations, including a kidney biopsy sample. Immunofluorescence results were negative biopsy. The patient had a past history of CKD (serum cre- for IgG, IgM, IgA, C3, and fibrinogen. No glomeruli were atinine, 0.83 mg/dL; estimated glomerular filtration rate, 49 detected in the electron microscopy specimen. According to mL/min/1.73 m2 at 6 months prior to this admission), hyper- the patient’s clinical course and pathological findings she tension, hyperlipidemia, and osteoarthritis of the knees, was diagnosed with APhN. which was treated with an ARB, calcium channel blocker, The patient’s serum creatinine levels gradually decreased fibrate, and NSAIDs. On admission to our hospital, her with rest and a low-sodium, low-protein diet for 1 week. blood pressure was 162/82 mmHg and her body temperature She was discharged from the hospital 8 days after admis- was 35.7℃. A physical examination only showed mild leg sion, with a serum creatinine level of 2.6 mg/dL, which had edema. Laboratory tests showed kidney dysfunction (blood further decreased to 1.6 mg/dL 1 year later. urea nitrogen, 45 mg/dL; serum creatinine, 3.49 mg/dL). Her electrolyte balance was normal, and no hypercalcemia Discussion or hyperphosphatemia was detected. Similarly, no inflamma- tory reaction, serum monoclonal protein, or autoimmune ab- Several studies have reported that the administration of normalities was detected. Urinary protein was 0.76 g daily OSP can result in AKI. Choi et al. investigated the relation- and there was no sign of hematuria. Urinary N-acetyl-beta- ship between OSP and AKI in a case-crossover study de- D-glucosaminidase and urinary β-2 microglobulin levels signed to remove confounding factors and concluded that were increased (33.1 U/L and 29,660 μg/L, respectively), OSP could cause AKI independent of any complications (3). suggesting tubulointerstitial damage. Fractional excretion of Furthermore, Haut et al. reported that a high-phosphate diet sodium was 2.4%. Urinary Bence Jones protein was nega- caused marked tubular injury in a rat nephrectomy CKD tive. A renal ultrasound examination showed bilateral, mild model, the pathological findings of which included damaged kidney swelling (left, 112×56 mm; right, 113×52 mm) with tubules with CPDs, interstitial fibrosis, tubular dilation and increased renal cortical echogenicity, indicating acute kidney inflammatory cell infiltration, resembling those in the cur- dysfunction (Fig. 1). No hydronephrosis or calcification was rent clinical case (4). These studies support the suggestion detected. that AKI in the current case was caused by OSP administra- An ultrasound-guided kidney biopsy was performed 15 tion. days after colonoscopy to determine the cause of her kidney Previous studies have reported two different clinical pat- dysfunction. The renal biopsy specimen was processed and terns of kidney injury following the administration of OSP examined by light microscopy, immunofluorescence, and bowel purgatives: acute and reversible kidney injury (ARKI) electron microscopy. Light microscopy sections were stained and APhN, which shows a delayed onset and is generally ir- with Hematoxylin and Eosin, periodic acid-Schiff, periodic reversible. ARKI occurs less than 1 day after the administra- acid-methenamine silver, Masson’s trichrome, and von tion of OSP and is accompanied by severe hyperphos- Kossa. Twelve glomeruli were observed, two of which re- phatemia and hypocalcemia leading to tetany, cardiac arrest, vealed global sclerosis, while no signs of glomerular hyper- and possible death. However, serum creatinine levels typi- cellularity, necrosis, crescent formation, mesangial cell pro- cally return to normal or near-normal levels. The renal- liferation, or thickening of the basement membrane were de- pathology findings of ARKI have not been reported to date. tected in the other 10 glomeruli. There was no evidence of In contrast, typical APhN progresses asymptomatically, and acute glomerular injury; however, obvious tubulointerstitial kidney dysfunction may thus remain undetected until several changes, including interstitial edema, focal inflammatory-cell days or even months after OSP administration.
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