Diagnostic Considerations

Pseudohyperphosphatemia is most commonly due to paraproteinemia from the following:

Waldenström macroglobulinemia
Multiple myeloma
Monoclonal gammopathy of unknown significance

Other differentials to be considered include the following:

Vitamin D intoxication
Oral saline laxative (Phospho-soda) abuse
Pseudohyperphosphatemia
Pseudohypoparathyroidism
Rhabdomyolysis

Differential Diagnoses

Workup

Prie D, Huart V, Bakouh N, Planelles G, Dellis O, Gerard B, et al. Nephrolithiasis and osteoporosis associated with hypophosphatemia caused by mutations in the type 2a sodium-phosphate cotransporter. N Engl J Med. 2002. 347:98991. [QxMD MEDLINE Link].
Segawa H, Onitsuka A, Kuwahata M, et al. Type IIc sodium-dependent phosphate transporter regulates calcium metabolism. J Am Soc Nephrol. 2009 Jan. 20(1):104-13. [QxMD MEDLINE Link]. [Full Text].
Collins JF, Bai L, Ghishan FK. The SLC20 family of proteins: dual functions as sodium-phosphate cotransporters and viral receptors. Pflugers Arch. 2004. 447:647-652. [QxMD MEDLINE Link].
Nowik M, Picard N, Stange G, et al. Renal phosphaturia during metabolic acidosis revisited: molecular mechanisms for decreased renal phosphate reabsorption. Pflugers Arch. 2008 Nov. 457(2):539-49. [QxMD MEDLINE Link].
Virkki LV, Biber J, Murer H, Forster IC. Phosphate transporters: a tale of two solute carrier families. Am J Physiol Renal Physiol. 2007. 293:F643-F654. [QxMD MEDLINE Link].
Shaikh A, Berndt T, Kumar R. Regulation of phospahte homeostasis by the phosphatonins and other novel mediators. Pediatr Nephrol. 2008. 23:1203-1210. [QxMD MEDLINE Link]. [Full Text].
Mirams M, Robinson BG, Mason RS, Nelson AE. Bone as a source of FGF23: regulation by phosphate?. Bone. 2004 Nov. 35(5):1192-9. [QxMD MEDLINE Link].
Liu S, Zhou J, Tang W, et al. Pathogenic role of Fgf23 in Hyp mice. Am J Physiol Endocrinol Metab. 2006 Jul. 291(1):E38-49. [QxMD MEDLINE Link].
Razzaque MS. FGF23-mediated regulation of systemic phosphate homeostasis: is Klotho an essential player. Am J Physiol Renal Physiol. 2009. 296:F470-F476. [QxMD MEDLINE Link]. [Full Text].
Pande S, Ritter CS, Rothstein M, et al. FGF-23 and sFRP-4 in chronic kidney disease and post-renal transplantation. Nephron Physiol. 2006. 104(1):p23-32. [QxMD MEDLINE Link].
Nishida Y, Taketani Y, Yamanaka-Okumura H, et al. Acute effect of oral phosphate loading on serum fibroblast growth factor 23 levels in healthy men. Kidney Int. 2006 Dec. 70(12):2141-7. [QxMD MEDLINE Link].
Sherman RA. Hyperphosphatemia in Dialysis Patients: Beyond Nonadherence to Diet and Binders. Am J Kidney Dis. 2016 Feb. 67 (2):182-6. [QxMD MEDLINE Link].
Prie D, Beck L, Urena P, Friedlander G. Recent findings in phosphate homeostasis. Curr Opin Nephrol Hypertens. 2005. 14:318-324. [QxMD MEDLINE Link].
Ichikawa S, Imel EA, Kreiter ML, et al. A homozygous missense mutation in human KLOTHO causes severe tumoral calcinosis. J Clin Invest. 2007 Sep. 117(9):2684-91. [QxMD MEDLINE Link]. [Full Text].
Ichikawa S, Sorenson AH, Austin AM, Mackenzie DS, Fritz TA, Moh A, et al. Ablation of the Galnt3 gene leads to low-circulating intact fibroblast growth factor 23 (Fgf23) concentrations and hyperphosphatemia despite increased Fgf23 expression. Endocrinology. 2009. 150:2543-2550. [QxMD MEDLINE Link]. [Full Text].
Lammoglia JJ, Mericq V. Familial tumoral calcinosis caused by a novel FGF23 mutation: response to induction of tubular renal acidosis with acetazolamide and the non-calcium phosphate binder sevelamer. Horm Res. 2009. 71:178-184. [QxMD MEDLINE Link].
Barbieri AM, Filopanti M, Bua G, Beck-Peccoz P. Two novel nonsense mutations in GALNT3 gene are responsible for familial tumoral calcinosis. J Hum Genet. 2007. 52:464-468. [QxMD MEDLINE Link].
Verdonck J, Geuens G, Delaere P, Vander Poorten V, Evenepoel P, Debruyne E. Surgical findings and post-operative parathormone levels in patients with secondary hyperparathyroidism. B-ENT. 2009. 5(3):143-8. [QxMD MEDLINE Link].
Tonelli M, Sacks F, Pfeffer M, Gao Z, Curhan G, Cholesterol and Recurrent Events Trial Investigators. Relation between serum phosphate level and cardiovascular event rate in people with coronary disease. Circulation. 2005. 112:2627-2633. [QxMD MEDLINE Link].
Shuto E, Taketani Y, Tanaka R, Harada N, Isshiki M, Sato M, et al. Dietary phosphorus acutely impairs endothelial function. J Am Soc Nephrol. 2009. 20:1504-1512. [QxMD MEDLINE Link]. [Full Text].
Shang D, Xie Q, Shang B, Zhang M, You L, Hao CM, et al. Hyperphosphatemia and hs-CRP Initiate the Coronary Artery Calcification in Peritoneal Dialysis Patients. Biomed Res Int. 2017. 2017:2520510. [QxMD MEDLINE Link]. [Full Text].
Sabbagh Y, Carpenter TO, Demay MB. Hypophosphatemia leads to rickets by impairing caspase-mediated apoptosis of hypertrophic chondrocytes. Proc Natl Acad Sci U S A. 2005 Jul 5. 102(27):9637-42. [QxMD MEDLINE Link]. [Full Text].
Rastogi A, Bhatt N, Rossetti S, Beto J. Management of Hyperphosphatemia in End-Stage Renal Disease: A New Paradigm. J Ren Nutr. 2020 May 5. [QxMD MEDLINE Link]. [Full Text].
Ball CL, Tobler K, Ross BC, Connors MR, Lyon ME. Spurious hyperphosphatemia due to sample contamination with heparinized saline from an indwelling catheter. Clin Chem Lab Med. 2004 Jan. 42(1):107-8. [QxMD MEDLINE Link].
Cachat F, Bardy D, Durussel C, Di Paolo E. Spurious hyperphosphatemia in a patient with alteplase-locked central venous catheter. Pediatr Nephrol. 2006 Feb. 21(2):301-2. [QxMD MEDLINE Link].
Marcu CB, Hotchkiss M. Pseudohyperphosphatemia in a patient with multiple myeloma. Conn Med. 2004 Feb. 68(2):71-2. [QxMD MEDLINE Link].
Larner AJ. Pseudohyperphosphatemia. Clin Biochem. 1995 Aug. 28(4):391-3. [QxMD MEDLINE Link].
Leehey DJ, Daugirdas JT, Ing TS, Reid RW. Spurious hyperphosphatemia due to hyperlipidemia. Arch Intern Med. 1985 Apr. 145(4):743-4. [QxMD MEDLINE Link].
Beloosesky Y, Grinblat J, Weiss A, et al. Electrolyte disorders following oral sodium phosphate administration for bowel cleansing in elderly patients. Arch Intern Med. 2003 Apr 14. 163(7):803-8. [QxMD MEDLINE Link].
Gumurdulu Y, Serin E, Ozer B, Gokcel A, Boyacioglu S. Age as a predictor of hyperphosphatemia after oral phosphosoda administration for colon preparation. J Gastroenterol Hepatol. 2004. 19:68-72. [QxMD MEDLINE Link].
Markowitz GS, Stokes MB, Radhakrishnan J, D'Agati VD. Acute phosphate nephropathy following oral sodium phosphate bowel purgative: an underrecognized cause of chronic renal failure. J Am Soc Nephrol. 2005. 16:3389-3396. [QxMD MEDLINE Link].
Markowitz GS, Nasr SH, Klein P, Anderson H, Stack JI, Alterman L, et al. Renal failure due to acute nephrocalcinosis following oral sodium phosphate bowel cleansing. Hum Pathol. 2004. 35:675-684. [QxMD MEDLINE Link].
Yoo KD, Kang S, Choi Y, Yang SH, Heo NJ, Chin HJ, et al. Sex, Age, and the Association of Serum Phosphorus With All-Cause Mortality in Adults With Normal Kidney Function. Am J Kidney Dis. 2015 Sep 2. [QxMD MEDLINE Link].
Connolly GM, Cunningham R, McNamee PT, Young IS, Maxwell AP. Elevated serum phosphate predicts mortality in renal transplant recipients. Transplantation. 2009. 87:1041-1044. [QxMD MEDLINE Link].
Tentori F, Blayney MJ, Albert JM, Gillespie BW, Kerr PG, Bommer J, et al. Mortality risk for dialysis patients with different levels of serum calcium, phosphorus, and PTH: the Dialysis Outcomes and Practice Patterns Study (DOPPS). Am J Kidney Dis. 2008. 52:519-530. [QxMD MEDLINE Link].
Hruska KA, Mathew S, Lund R, Qiu P, Pratt R. Hyperphosphatemia of chronic kidney disease. Kidney International. 2008. 74:148-157. [QxMD MEDLINE Link]. [Full Text].
[Guideline] Ketteler M, Block GA, Evenepoel P, Fukagawa M, Herzog CA, McCann L, et al. Executive summary of the 2017 KDIGO Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) Guideline Update: what's changed and why it matters. Kidney Int. 2017 Jul. 92 (1):26-36. [QxMD MEDLINE Link]. [Full Text].
Isakova T, Gutiérrez OM, Chang Y, et al. Phosphorus binders and survival on hemodialysis. J Am Soc Nephrol. 2009 Feb. 20(2):388-96. [QxMD MEDLINE Link]. [Full Text].
Block GA, Wheeler DC, Persky MS, et al. Effects of phosphate binders in moderate CKD. J Am Soc Nephrol. 2012 Aug. 23(8):1407-15. [QxMD MEDLINE Link]. [Full Text].
Shutto Y, Shimada M, Kitajima M, Yamabe H, Saitoh Y, Saitoh H, et al. Inadequate Awareness among Chronic Kidney Disease Patients Regarding Food and Drinks Containing Artificially Added Phosphate. PLoS One. 2013 Nov 13. 8(11):e78660. [QxMD MEDLINE Link]. [Full Text].
Marraffa JM, Hui A, Stork CM. Severe hyperphosphatemia and hypocalcemia following the rectal administration of a phosphate-containing Fleet pediatric enema. Pediatr Emerg Care. 2004 Jul. 20(7):453-6. [QxMD MEDLINE Link].
[Guideline] Hawley C. Serum phosphate. Nephrology. Apr 2006. 11(S1):S201-5.
Sutherland SM, Hong DK, Balagtas J, Gutierrez K, Dvorak CC, Sarwal M. Liposomal amphotericin B associated with severe hyperphosphatemia. Pediatr Infect Dis J. 2008 Jan. 27(1):77-9. [QxMD MEDLINE Link].
Vervloet MG, Sezer S, Massy ZA, Johansson L, Cozzolino M, Fouque D, et al. The role of phosphate in kidney disease. Nat Rev Nephrol. 2017 Jan. 13 (1):27-38. [QxMD MEDLINE Link].
Ix JH, Anderson CA, Smits G, Persky MS, Block GA. Effect of dietary phosphate intake on the circadian rhythm of serum phosphate concentrations in chronic kidney disease: a crossover study. Am J Clin Nutr. 2014 Nov. 100 (5):1392-7. [QxMD MEDLINE Link]. [Full Text].
Graham-Brown MP, Churchward DR, Smith AC, Baines RJ, Burton JO. A 4-month programme of in-centre nocturnal haemodialysis was associated with improvements in patient outcomes. Clin Kidney J. 2015 Dec. 8 (6):789-795. [QxMD MEDLINE Link]. [Full Text].
Dey V, Hair M, So B, Spalding EM. Thrice-Weekly Nocturnal In-Centre Haemodiafiltration: A 2-Year Experience. Nephron Extra. 2015 May-Aug. 5 (2):50-7. [QxMD MEDLINE Link]. [Full Text].
Ketteler M. Phosphate Metabolism in CKD Stages 3-5: Dietary and Pharmacological Control. Int J Nephrol. 2011. 2011:970245. [QxMD MEDLINE Link]. [Full Text].
Akizawa T, Kameoka C, Kaneko Y, Kawasaki S. Long-term treatment of hyperphosphatemia with bixalomer in Japanese hemodialysis patients. Ther Apher Dial. 2013 Dec. 17(6):612-9. [QxMD MEDLINE Link].
Sekercioglu N, Thabane L, Díaz Martínez JP, Nesrallah G, Longo CJ, Busse JW, et al. Comparative Effectiveness of Phosphate Binders in Patients with Chronic Kidney Disease: A Systematic Review and Network Meta-Analysis. PLoS One. 2016 Jun 8. 11 (6):e0156891. [QxMD MEDLINE Link]. [Full Text].
Pai AB, Jang SM, Wegrzyn N. Iron-based phosphate binders--a new element in management of hyperphosphatemia. Expert Opin Drug Metab Toxicol. 2016. 12 (1):115-27. [QxMD MEDLINE Link].
Ketteler M, Liangos O, Biggar PH. Treating hyperphosphatemia - current and advancing drugs. Expert Opin Pharmacother. 2016 Oct. 17 (14):1873-9. [QxMD MEDLINE Link].
Kling J. New Phosphate Binder for Renal Failure Lowers Pill Burden. Medscape Medical News. Jun 4 2013. Available at http://www.medscape.com/viewarticle/805262. Accessed: Dec 26 2013.
Brooks M. FDA Clears New Phosphate Binder Velphoro. Medscape Medical News. Dec 3 2013. Available at http://www.medscape.com/viewarticle/815337. Accessed: Jan 3 2014.
Sprague SM, Floege J. Sucroferric oxyhydroxide for the treatment of hyperphosphatemia. Expert Opin Pharmacother. 2018 Jul. 19 (10):1137-1148. [QxMD MEDLINE Link].
Koiwa F, Yokoyama K, Fukagawa M, Akizawa T. Evaluation of changes in ferritin levels during sucroferric oxyhydroxide treatment. Clin Kidney J. 2019 Apr. 12 (2):294-299. [QxMD MEDLINE Link]. [Full Text].
Floege J, Covic AC, Ketteler M, Mann JF, Rastogi A, Spinowitz B, et al. Long-term effects of the iron-based phosphate binder, sucroferric oxyhydroxide, in dialysis patients. Nephrol Dial Transplant. 2015 Jun. 30 (6):1037-46. [QxMD MEDLINE Link].
Spaia S. Phosphate binders: Sevelamer in the prevention and treatment of hyperphosphataemia in chronic renal failure. Hippokratia. 2011 Jan. 15:22-6. [QxMD MEDLINE Link]. [Full Text].
Vemuri N, Michelis MF, Matalon A. Conversion to lanthanum carbonate monotherapy effectively controls serum phosphorus with a reduced tablet burden: a multicenter open-label study. BMC Nephrol. 2011 Sep 30. 12:49. [QxMD MEDLINE Link]. [Full Text].
Lewis JB, Sika M, Koury MJ, Chuang P, Schulman G, Smith MT, et al. Ferric Citrate Controls Phosphorus and Delivers Iron in Patients on Dialysis. J Am Soc Nephrol. 2014 Jul 24. [QxMD MEDLINE Link].
Frazao JM, Adragao T. Treatment of hyperphosphatemia with sevelamer hydrochloride in dialoysis patients: effects on vascular calcification, bone and a close look into the survival data. Kidney Int Suppl. 2008. 111:S38-S43. [QxMD MEDLINE Link].
Sprague SM. A comparative review of the efficacy and safety of established phosphate binders: calcium, sevelamer, and lanthanum carbonate. Curr Med Res Opin. 2007 Dec. 23(12):3167-75. [QxMD MEDLINE Link].
Marangon N, Lindholm B, Stenvinkel P. Nonphosphate-binding effects of sevelamer--are they of clinical relevance?. Semin Dial. 2008. 21:385-389. [QxMD MEDLINE Link].
Takei T, Otsubo S, Uchida K, et al. Effects of sevelamer on the progression of vascular calcification in patients on chronic haemodialysis. Nephron Clin Pract. 2008. 108(4):c278-83. [QxMD MEDLINE Link].
Taketani Y, Koiwa F, Yokoyama K. Management of phosphorus load in CKD patients. Clin Exp Nephrol. 2017 Mar. 21 (Suppl 1):27-36. [QxMD MEDLINE Link].
Barreto DV, Barreto FdeC, de Carvalho AB, Cuppari L, Draibe SA, Dalboni MA, et al. Phosphate binder impact on bone remodeling and coronary calcification -- results from the BRIC study. Nephron Clin Pract. 2008. 110:c278-c283. [QxMD MEDLINE Link].
Habbous S, Przech S, Acedillo R, Sarma S, Garg AX, Martin J. The efficacy and safety of sevelamer and lanthanum versus calcium-containing and iron-based binders in treating hyperphosphatemia in patients with chronic kidney disease: a systematic review and meta-analysis. Nephrol Dial Transplant. 2017 Jan 1. 32 (1):111-125. [QxMD MEDLINE Link].
Labonté ED, Carreras CW, Leadbetter MR, Kozuka K, Kohler J, Koo-McCoy S, et al. Gastrointestinal Inhibition of Sodium-Hydrogen Exchanger 3 Reduces Phosphorus Absorption and Protects against Vascular Calcification in CKD. J Am Soc Nephrol. 2015 May. 26 (5):1138-49. [QxMD MEDLINE Link]. [Full Text].
Block GA, Bleyer AJ, Silva AL, Weiner DE, Lynn RI, Yang Y, et al. Safety and Efficacy of Tenapanor for Long-term Serum Phosphate Control in Maintenance Dialysis: A 52-Week Randomized Phase 3 Trial (PHREEDOM). Kidney360. 2021 Oct 28. 2 (10):1600-1610. [QxMD MEDLINE Link]. [Full Text].
Pergola PE, Rosenbaum DP, Yang Y, Chertow GM. A Randomized Trial of Tenapanor and Phosphate Binders as a Dual-Mechanism Treatment for Hyperphosphatemia in Patients on Maintenance Dialysis (AMPLIFY). J Am Soc Nephrol. 2021 Jun 1. 32 (6):1465-1473. [QxMD MEDLINE Link]. [Full Text].
Block GA, Rosenbaum DP, Yan A, Chertow GM. Efficacy and Safety of Tenapanor in Patients with Hyperphosphatemia Receiving Maintenance Hemodialysis: A Randomized Phase 3 Trial. J Am Soc Nephrol. 2019 Apr. 30 (4):641-652. [QxMD MEDLINE Link]. [Full Text].
Pergola PE, Rosenbaum DP, Yang Y, Chertow GM. A Randomized Trial of Tenapanor and Phosphate Binders as a Dual-Mechanism Treatment for Hyperphosphatemia in Patients on Maintenance Dialysis (AMPLIFY). J Am Soc Nephrol. 2021 Jun 1. 32 (6):1465-1473. [QxMD MEDLINE Link]. [Full Text].
King AJ, Kohler J, Fung C, Jiang Z, Quach A, Kumaraswamy P, et al. Combination treatment with tenapanor and sevelamer synergistically reduces urinary phosphorus excretion in rats. Am J Physiol Renal Physiol. 2021 Jan 1. 320 (1):F133-F144. [QxMD MEDLINE Link]. [Full Text].
Hansen D, Rasmussen K, Danielsen H, Meyer-Hofmann H, Bacevicius E, Lauridsen TG, et al. No difference between alfacalcidol and paricalcitol in the treatment of secondary hyperparathyroidism in hemodialysis patients: a randomized crossover trial. Kidney Int. 2011 Oct. 80(8):841-50. [QxMD MEDLINE Link].

Media Gallery

Approximately 60-70% of dietary phosphate, 1000-1500 mg/day, is absorbed in the small intestine. Although vitamin D can enhance the absorption, especially under conditions of dietary phosphate depletion, intestinal phosphate absorption does not require the presence of active vitamin D. Specifically, high serum phosphate and high dietary phosphate intake do not significantly impair intestinal uptake. The movement of phosphate in and out of bone, the reservoir containing most of the total body phosphate, is generally balanced. Renal excretion of excess dietary phosphate intake ensures maintenance of phosphate homeostasis, maintaining serum phosphate at a level of approximately 3-4 mg/dL in the serum.
The vast majority of filtered phosphate is reabsorbed by type 2a sodium phosphate cotransporters located on the apical membrane of the renal proximal tubule. The expression of these cotransporters is increased by low dietary phosphate intake and several growth factors to enhance phosphate absorption. The expression is decreased by high dietary phosphate intake, parathyroid hormone (PTH), FGF23, and dopamine. Phosphate absorption in the remainder of the nephron is generally mediated by type 3 sodium phosphate cotransporters. No direct evidence has been found related to the regulation of these transporters in renal cells under physiologic conditions. The absorption in the proximal tubule is regulated such that the final excretion matches the dietary excess in order to maintain homeostasis.
Hyperphosphatemia inhibits 1-alpha hydroxylase in the proximal tubule directly and indirectly through stimulation of FGF23, thus inhibiting the conversion of 25-hydroxy vitamin D3 to the active metabolite, 1,25 dihydroxyvitamin D3. FGF23 additionally increases the expression of 24-hydroxylase, leading to inactivation of active 1,25 dihydroxyvitamin D3. The decrease in active vitamin D production with high phosphate is somewhat offset by the ability of hyperphosphatemia to stimulate the secretion of parathyroid hormone (PTH), which will increase the activity of 1-alpha hydroxylase. The result is generally a neutral effect on intestinal phosphate absorption. Hyperphosphatemia-stimulated PTH secretion is mediated through an as yet unidentified pathway. With normal renal function, the transient increase in PTH and decrease in vitamin D serve to inhibit renal and intestinal absorption of phosphate, resulting in resolution of the hyperphosphatemia. In contrast, under conditions of renal failure, sustained hyperphosphatemia results in sustained hyperparathyroidism. The hyperparathyroidism enhances renal phosphate excretion but also enhances bone resorption, releasing more phosphate into the serum. As renal failure progresses and the ability of the kidney to excrete phosphate continues to diminish, the action of PTH on the bone can exacerbate the already present hyperphosphatemia.

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Author

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Society of Nephrology<br/>Received income in an amount equal to or greater than $250 from: Healthcare Quality Strategies, Inc.

Coauthor(s)

Rosemary Ouseph, MD Professor of Medicine, Director of Kidney Transplant, University of Louisville School of Medicine

Rosemary Ouseph, MD is a member of the following medical societies: American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplant Surgeons

Disclosure: Nothing to disclose.

Vibha Nayak, MD Assistant Professor of Nephrology, Director of Home Dialysis, Kidney Disease Program, University of Louisville School of Medicine

Vibha Nayak, MD is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FASN Professor of Medicine, Section of Nephrology-Hypertension, Deming Department of Medicine, Tulane University School of Medicine

Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Acknowledgements

Jeffrey L Arnold, MD, FACEP Chairman, Department of Emergency Medicine, Santa Clara Valley Medical Center

Jeffrey L Arnold, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physicians

Disclosure: Nothing to disclose. Andrew J Dailey, MD Fellow, Department of Medicine, Division of Nephrology, University of Louisville School of Medicine