eMedicine Specialties > Nephrology > Tubulointerstitial Diseases of the Kidney

Nephrocalcinosis

Author: Tibor Fulop, MD, Assistant Professor, Department of Internal Medicine, Division of Nephrology, University of Mississippi Medical Center
Coauthor(s): Mahendra Agraharkar, MD, MBBS, FACP, FASN, Clinical Associate Professor of Medicine, Baylor College of Medicine, President & CEO, Space City Associates of Nephrology; Rupert Patel, MD, Physician, Division of Nephrology, Houston, Texas; Rajiv Gupta, MD, Assistant Professor, Department of Medicine, Texas A & M University Health Science Center; Consulting Staff, Veterans Affairs Medical Center
Contributor Information and Disclosures

Updated: Apr 21, 2009

Introduction

Background

Nephrocalcinosis is a condition in which calcium levels in the kidneys are increased. This increase can be detected (usually as an incidental finding) through a radiologic exam or via microscopic examination of the renal tissues. The term nephrocalcinosis most often applies to a generalized increase in renal calcium content, as opposed to the localized increase observed in calcified renal infarct and caseating granulomas of renal tuberculosis.1 (See image below and Image 1.)

Diagram of a nephron.

Diagram of a nephron.

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Diagram of a nephron.

Diagram of a nephron.


Microscopic nephrocalcinosis is characterized by the presence of microscopic crystalline calcium precipitates in the form of oxalate and/or phosphate. Patients with macroscopic nephrocalcinosis have larger areas of calcifications, which can be observed on visual or radiologic examination without further magnification.

Nephrocalcinosis has a significant overlap with hypercalcemia, nephrolithiasis, renal parenchymal damage, and reduced renal function. Therefore, rather being considered a single, distinct disease process, it should be viewed as a helpful finding for several distinct disease processes, demanding further evaluation. (See images below and Images 2-4.)

Nephrocalcinosis.

Nephrocalcinosis.

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Nephrocalcinosis.

Nephrocalcinosis.


Nephrocalcinosis.

Nephrocalcinosis.

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Nephrocalcinosis.

Nephrocalcinosis.


Nephrocalcinosis.

Nephrocalcinosis.

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Nephrocalcinosis.

Nephrocalcinosis.


Pathophysiology

Hypercalcemic nephropathy 

Patients with hypercalcemia develop renal function abnormalities. Under these circumstances, the term hypercalcemic nephropathy is more appropriate than is the older term chemical nephrocalcinosis.

Calcium is a critical divalent cation that is transported, along with sodium, potassium, and water, in a complex and regulated manner along the renal tubular epithelium. The cytoplasmic concentration of calcium is tightly regulated and kept very low, being maintained by active extracellular extrusion of calcium and sequestration into the endoplasmic reticulum and mitochondria. Increased extracellular calcium leads to impairment of the calcium messenger system with gross tubular impairment. The effects of increased calcium have been studied extensively in rats. Rats treated with vitamin D demonstrated mitochondrial swelling and loss of mitochondrial enzyme activities before calcification appeared. Parathyroid extract induced hypercalcemia was found to cause changes in rat kidneys, predominately affecting the distal nephron, with focal necrosis of the outer medullary collecting ducts and the ascending limb of the loop of Henle.

Hypercalcemia results in renal vasoconstriction and a reduced glomerular filtration rate. It also interferes with renal tubular functions. Impaired renal concentration ability and resistance to vasopressin are the most common defects observed with hypercalcemia. This may be mediated by reduced sodium transport in the loop of Henle and by antidiuretic hormone antagonism via calcium-sensing receptors,2 or it may be related to medullary prostaglandin synthesis. Maximum diluting capacity remains unimpaired. Effectively, the sum effect of this will be a clinical picture equivalent to that of nephrogenic diabetes insipidus.

Renal sodium conservation is also impaired because of reduced absorption of sodium chloride in the medullary thick ascending limb and collecting tubule, although this rarely results in gross renal sodium losses. Potassium excretion is increased. Magnesium excretion is also increased; the effect probably is due to suppression of the parathyroid hormone, which enhances tubular magnesium absorption.3 Hypercalcemia increases urinary calcium excretion by increasing the filtered load and reducing tubular absorption. Its effects on phosphate excretion are complex. In experimental animals, pure hypercalcemia reduces phosphate excretion; conversely, in certain cancers, it can be associated with increased phosphate excretion, but the latter occurrence is probably due to the presence of phosphaturic peptides (phosphatonins), which are secreted in some malignancies.4,5

The effects on the acid-base balance are even more complex. Increased renal acid excretion occurs with intravenous calcium infusions, and metabolic alkalosis frequently has been reported in patients with hypercalcemia. On the other hand, parathyroid hormone decreases hydrogen ion excretion, leading to a distal type of renal tubular acidosis (RTA). This opposing effect of hypercalcemia and parathyroid hormone has been used in the differential diagnosis of hypercalcemia, because serum bicarbonate is lower and chloride is higher when hyperparathyroidism is the cause of hypercalcemia.

Microscopic nephrocalcinosis

Microscopic nephrocalcinosis has undergone elaborate laboratory study. Although the condition is a theoretical stage between hypercalcemia and macroscopic nephrocalcinosis, it is difficult to demonstrate in humans, because renal biopsies are not routinely performed in the early stages of metabolic diseases known to lead to the macroscopic stage. However, some elegant human data now exists that demonstrates early stone formation, with blockage of the collecting tubes and subsequent inflammatory response.6 At autopsy, healthy human kidneys invariably contain microscopic deposits of calcium in the renal medulla. Microscopic nephrocalcinosis can occur without macroscopic involvement in patients with longstanding hypercalcemia from primary parathyroidism, milk-alkali syndrome, and primary hyperoxaluria.

Different patterns of microscopic nephrocalcinosis have been described. Cortical calcification has been found after parenteral calcium administration. The corticomedullary type involves calcium phosphate deposits that occur in the inner zone of the renal cortex and extend into the medulla. Precipitating factors include excess parathyroid hormone, vitamin D, acetazolamide, magnesium depletion, decreased urinary citrate, and hypothyroid state. Increased plasma calcium is not an essential prerequisite for this type of nephrocalcinosis. The medullary pattern has been reported in hyaline droplet nephropathy due to the inhalation of volatile hydrocarbons. The pelvic type affects renal papillae. The deposits usually are calcium phosphate, but calcium oxalate also has been implicated. The underlying mechanism appears to be either increased intestinal absorption or decreased renal excretion of calcium.

Macroscopic nephrocalcinosis

Macroscopic nephrocalcinosis refers to calcium deposition that is visible without magnification and usually is discovered through conventional radiography, ultrasonography, or computed tomography (CT) scanning, or at autopsy. Macroscopic nephrocalcinosis can affect either the cortex or medulla, with the latter site being more common. (See images below and Images 5, 6.)

Nonenhanced coronal computed tomography scans thr...

Nonenhanced coronal computed tomography scans through the kidneys. These images show cortical and medullary nephrocalcinosis (left kidney). Both kidneys appear scarred. Note the thinning of the renal cortex at the upper pole of the left kidney. This patient gave a long history of chronic pyelonephritis, which is an unusual cause of nephrocalcinosis.

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Nonenhanced coronal computed tomography scans thr...

Nonenhanced coronal computed tomography scans through the kidneys. These images show cortical and medullary nephrocalcinosis (left kidney). Both kidneys appear scarred. Note the thinning of the renal cortex at the upper pole of the left kidney. This patient gave a long history of chronic pyelonephritis, which is an unusual cause of nephrocalcinosis.


Axial computed tomography scans obtained from a p...

Axial computed tomography scans obtained from a patient with a long history of renal tubular acidosis. These images show bilateral medullary nephrocalcinosis (early arterial phase).

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Axial computed tomography scans obtained from a p...

Axial computed tomography scans obtained from a patient with a long history of renal tubular acidosis. These images show bilateral medullary nephrocalcinosis (early arterial phase).


Cortical nephrocalcinosis is rare and usually occurs secondary to diffuse cortical disease injury. The calcification can be patchy or confluent. In chronic glomerulonephritis, calcium deposits  are found most often in periglomerular tissue and not in the glomerulus. Nephrocalcinosis also has been reported in familial infantile nephrotic syndrome and in Alport syndrome. Acute cortical necrosis secondary to toxemia of pregnancy, snakebite, or hemolytic-uremic syndrome can lead to patchy cortical nephrocalcinosis. Calcium deposition can start as early as 30 days after cortical necrosis. Chronic pyelonephritis and vesicoureteral reflux are also implicated.7  Rare etiologies of cortical nephrocalcinosis include renal transplantation, primary hyperoxaluria, methoxyflurane abuse, autosomal recessive polycystic kidney disease, and benign nodular cortical nephrocalcinosis.

Medullary nephrocalcinosis assumes the form of small nodules of calcification clustered in each pyramid. (See first image below and Image 7.) Diagnosing the underlying renal disease based on the appearance is difficult. Characteristic exceptions include papillary necrosis due to analgesic abuse and medullary sponge kidneys.8 (See second and third images below and Images 8, 9.) In papillary necrosis, the entire papilla may be calcified, while in medullary sponge kidney, there is a characteristic band of calcification in the renal pyramids. It has been suggested that when hypercalcemia is the most important factor, the first foci of calcification develop in the renal tubular cells, and that when hypercalciuria is the major factor, they form in the interstitium.

Ultrasonogram of the right kidney in a woman with...

Ultrasonogram of the right kidney in a woman with nephrocalcinosis. This image shows hyperechoic foci in the pyramids.

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Ultrasonogram of the right kidney in a woman with...

Ultrasonogram of the right kidney in a woman with nephrocalcinosis. This image shows hyperechoic foci in the pyramids.


Excretory urogram obtained at 15 minutes in a man...

Excretory urogram obtained at 15 minutes in a man with renal papillary necrosis, most likely a patient with diabetes mellitus and repeated urinary tract infections. This image shows bilateral hydronephrosis and a hydroureter due to obstruction by sloughed papillae at the lower end of the ureter.

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Excretory urogram obtained at 15 minutes in a man...

Excretory urogram obtained at 15 minutes in a man with renal papillary necrosis, most likely a patient with diabetes mellitus and repeated urinary tract infections. This image shows bilateral hydronephrosis and a hydroureter due to obstruction by sloughed papillae at the lower end of the ureter.


Plain kidney, ureters, and bladder (KUB) radiogra...

Plain kidney, ureters, and bladder (KUB) radiograph in a man with renal papillary necrosis, most likely a patient with diabetes mellitus and repeated urinary tract infections. This image shows bilateral renal calcification. A large, sloughed, and calcified renal papilla is present in the region of left vesicoureteric junction. Note the 2 pelvic phleboliths opposite the ischial spine on the right.

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Plain kidney, ureters, and bladder (KUB) radiogra...

Plain kidney, ureters, and bladder (KUB) radiograph in a man with renal papillary necrosis, most likely a patient with diabetes mellitus and repeated urinary tract infections. This image shows bilateral renal calcification. A large, sloughed, and calcified renal papilla is present in the region of left vesicoureteric junction. Note the 2 pelvic phleboliths opposite the ischial spine on the right.


Intraluminal tubular calcium crystals are believed to serve as potential nidi for further build-up of calcium and other stone-forming substances, including oxalate and uric acid. Whether further growth of nephroliths occurs probably depends on a number of additional factors, such as abnormal urine composition, urine flow and volume, and the presence or absence of endogenous inhibitors of crystalline formation in the urine. 

Mortality/Morbidity

The morbidity and mortality associated with nephrocalcinosis is dependent on the disease associated with the condition rather than on the nephrocalcinosis itself.

Clinical

History

The underlying etiology primarily determines the presentation of nephrocalcinosis, although in many cases, the condition remains asymptomatic and is identified only as a radiologic abnormality. Potential clinical features include the following:

  • Clinical features of hypercalcemia
    • Relative vasopressin resistance with decreased renal concentrating ability and increased free water diuresis (nephrogenic diabetes insipidus), manifesting as polyuria and polydipsia.
    • Other defects, such as renal glycosuria, reduced glucose tubular maximal, aminoaciduria, and nonglomerular proteinuria have occasionally been reported.
    • Reversible hypertension occurs in approximately 50% of patients, due to increased peripheral vasoconstriction.
    • Hypercalcemia is also a well-established cause of renal failure, due to direct renal vasoconstriction and to volume depletion induced by excessive diuresis. This usually is reversible, with normal renal function returning as the hypercalcemia is corrected with volume replacement. However, irreversible failure can occur with long-standing hypercalcemia and is always associated with calcium crystal deposition.
  • Clinical features of microscopic nephrocalcinosis
    • A few studies describe the effects of nephrocalcinosis on renal function in rats.9 Various investigators have observed reduced concentration capacity, increased blood urea nitrogen (BUN), and prolongation of a single nephron transit time in a distal tubule,10  although no detailed studies of glomerular filtration or renal tubular function exist in these models.
    • Occasionally, rats with the pelvic type of nephrocalcinosis may develop acute pyelonephritis or calculous ureteral obstruction with renal failure.
    • However, nephrocalcinosis in rats is a poor model for humans because of the high incidence of spontaneous glomerulosclerosis in laboratory rats, the different distribution of calcium in the kidney, and the absence of a rat model for many of the diseases that cause human nephrocalcinosis.
  • Clinical features of macroscopic nephrocalcinosis
    • A wide range of abnormalities can occur with medullary nephrocalcinosis. Calcium nodules may rupture through the papillary epithelium into the calyceal system to become urinary stones and elicit the clinical presentations of renal colic, hematuria, passage of urinary stones, or urinary tract infection. However, macroscopic nephrocalcinosis should not be considered synonymous with urinary stones, because nephrocalcinosis usually implies a more profound metabolic derangement.
    • Polyuria and polydipsia may be prominent because of the excess of free water diuresis with reduced renal concentrating ability. 
    • Hypertension is relatively less common, probably reflecting a reduced ability to conserve sodium.
    • Proteinuria may be observed, although it is in the nonnephrotic range and usually is less than 500 mg per day.
    • In Dent disease, loss of low – molecular weight proteins may exceed 2 grams per day. Hypercalciuria, nephrolithiasis, and nephrocalcinosis are some additional presenting features.
    • Microscopic pyuria is frequently found and represents a chronic inflammatory response to medullary calcification.
    • Distal tubular dysfunction is common with a mild salt-losing defect; this defect may become obvious only with profound decrease of per os intake (anorexia) or when another source salt-water loss emerges, such us diarrhea or vomiting.
    • Proximal tubular dysfunction is unusual, except for tubular proteinuria and the aminoaciduria of Dent disease.
    • Medullary nephrocalcinosis of any etiology can cause secondary distal tubular acidosis related to distal tubular calcium deposition and chronic inflammation in the medulla.
    • Patients may present with renal failure or with features of their underlying disease.

Physical

The physical findings are nonspecific and reflect the underlying disorders responsible for nephrocalcinosis.

Causes

  • Primary hyperparathyroidism is the single most common cause of nephrocalcinosis in adults. While nephrocalcinosis is a relatively rare complication (5%), primary hyperparathryroidism is relatively common, especially in the elderly. Nephrocalcinosis itself is related more to the duration than to the intensity of hypercalcemia. The classic clinical findings are sometimes referred to as "(abdominal) groans, stones, and bones." This common phrase is a reminder that patients may present with kidney stones, bone pain, osteoporosis, and pathologic fractures, all of which can result in abdominal discomfort. Rarely, hyperparathyroidism can be associated with multiple endocrine neoplasia type 1 (MEN1).
  • Distal RTA is the second most common cause of medullary nephrocalcinosis. The familial form and the secondary form (autoimmune-associated anti-K/H channel antibody) have a high incidence.11 The contributing mechanisms to nephrocalcinosis in distal RTA are hypercalcemia, hypercalciuria, metabolic acidosis, and reduced excretion of citrate in the presence of increased urinary pH. Because medullary nephrocalcinosis can itself be a cause of distal RTA, separating out the initial insult can be difficult. Renal function is fairly well maintained.
  • Other causes of nephrocalcinosis are hypervitaminosis-D states12 resulting from excessive treatment of hypoparathyroidism, self-administration of vitamins, and the presence of a granulomatous disease, such as sarcoidosis.13  In granulomatous disorders, there is an increased conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol in the granuloma, resulting in an unregulated production of bioactive vitamin D with resultant excessive intestinal absorption of calcium and phosphorus. In addition, cytokines (IL-2) released in these disorders cause dysregulation of calcium homeostasis and activation of osteoclasts, resulting in subacute and chronic hypercalcemia.
  • Any other cause of hypercalcemia, particularly when associated with hypercalciuria, can be a contributor to nephrocalcinosis. Etiologies include milk-alkali syndrome (due to excess ingestion of antacids, in the modern era with CaCO 3 supplements), hyperparathyroidism, and malignant disease (due to bone involvement and humoral factors, including cytokines and parathyroid hormone – related peptide). Idiopathic hypercalciuria,14 a common metabolic disease, also is known to cause nephrocalcinosis.
  • Nephrocalcinosis and renal failure are increasingly being recognized as common complications of phosphate supplementation, particularly in the elderly.15,16,17,18,19 Other possible risk factors are preexisting renal failure, high blood pressure, and the treatment of high blood pressure (with angiotensin-converting enzyme [ACE] inhibitors or angiotensin-receptor blockers). Phosphate supplements may contribute to renal calcifications in children with hypophosphatemic rickets. In vitro studies have shown that an increased urinary concentration of phosphate can result in intratubular crystallization with altered solubility.
  • Medullary sponge kidney is a common cause of medullary calcification, with calcium lying in dilated collecting ducts rather than in the renal substance. These ectatic outpouchings are believed to be areas of urinary stasis possessing the ideal milieu for the formation of these calcifying complexes. The calcium deposits are larger and more sharply defined than they are in metabolic disease, and they are uneven in distribution.8 Associated hemihypertrophy of the body may exist. Unlike the severe renal damage with minimal calcification associated with hypercalcemic states, nephrocalcinosis associated with distal RTA and medullary sponge kidney usually is gross, and renal function is relatively well preserved.
  • Renal papillary necrosis associated with analgesic nephropathy is identified as calcified papillae rather than as a speckled pattern.
  • Other associations with nephrocalcinosis include rapidly progressive osteoporosis due to immobilization, menopause, aging, or steroids.
  • Primary (familial) hyperoxaluria, or secondary hyperoxaluria due to increased intake of oxalates, enhanced absorption due to intestinal disease, or ingestion of ethylene glycol or methoxyflurane can induce medullary calcification.20,21 Primary hyperoxaluria and ethylene glycol intoxication is also associated with diffuse calcium-oxalate depositions in many other organs, including the eye and the heart.
  • Chronic hypokalemic states, such as Bartter syndrome, primary hyperaldosteronism, Liddle syndrome, and 11-beta hydroxylase deficiency, are associated with reduced urine citrate excretion and tubular epithelial damage, leading to calcium precipitations.
  • Autosomal dominant hypophosphatemic rickets and X-linked hypophosphatemic conditions22  have been associated abnormal phosphate wastage and nephrocalcinosis due to elevated levels of phosphatonins (fibroblast growth factor 23; secreted frizzled-related protein 4).4,5 Nephrocalcinosis is very common (~80% on ultrasonography) and may be associated with phosphate supplementation for the condition.
  • Dent disease and familial magnesium-losing nephropathy are rare inherited diseases causing medullary calcification.
    • Dent disease arises from a defect in a gene on the short arm of the X chromosome that codes for the renal chloride channel in the proximal tubule (CLC-5). This disease is referred to by several other names in the international literature, including X-linked recessive hypophosphatemic rickets (Italy), X-linked recessive nephrolithiasis, and idiopathic low-molecular weight proteinuria with hypercalciuria and nephrocalcinosis (Japan). Mutations in the OCRL-1 gene — normally associated with Lowe's syndrome — have been described in cases of clinical Dent disease, expanding the potential for genetic diversity.23
    • Inherited forms of magnesium-losing nephropathy have been described.24 Familial hypomagnesemia hypocalciuric nephrocalcinosis (FHHNC) is an autosomal recessive disease associated with cation loss through a defect in renal tight junctions protein (paracellin-1) involved in paracellular transport.25,26
  • Associated malignancies are not typical in nephrocalcinosis, because patients seldom survive long enough with hypercalcemia to develop them; one possible exception is the parathyroid carcinoma.
  • Familial benign hypercalcemia and hyperthyroidism are not associated with renal calcification.
  • Premature, sick infants have been observed to develop diffuse nephrocalcinosis (about 2/3 among infants born <1500 g), typically when exposed to diuretic therapy or prolonged O 2 therapy. There is no clearly effective therapy.27 While these lesions may improve later on,28 the natural history of this phenomenon is not well understood.
  • There has been a growing awareness of the diffusely increased calcifications in patients with advanced renal failure and end-stage renal disease.29  In the uremic environment, the presence of large, pharmacologic dose vitamin-D analogs and calcium-based phosphorus binders appear to accelerate the process. It appears that the presence of extraskeletal calcifications is more closely correlated with calcium x phosphorus product (sometimes referred to as the "double product") and total-body calcium overload then with the presence of serum hypercalcemia. Calcifications are not limited to the kidneys but involve multiple organs, including the heart, vascular beds, parenchymal organs, skin, and subcutaneous tissues.

More on Nephrocalcinosis

Overview: Nephrocalcinosis
Differential Diagnoses & Workup: Nephrocalcinosis
Treatment & Medication: Nephrocalcinosis
Follow-up: Nephrocalcinosis
Multimedia: Nephrocalcinosis
References
Further Reading
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References

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  33. Barre PE, Gascon-Barre M, Meakins JL, et al. Hydroxychloroquine treatment of hypercalcemia in a patient with sarcoidosis undergoing hemodialysis. Am J Med. Jun 1987;82(6):1259-62. [Medline].

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Keywords

nephrocalcinosis, kidney, kidneys, kidney stones, kidney stone, hypercalcemia, hypercalciuria, hyperparathyroidism, nephrolithiasis, urinary stones, urinary stone, medullary nephrocalcinosis, crystal-induced nephropathy, increase in renal calcium content, microscopic nephrocalcinosis, macroscopic nephrocalcinosis, hypercalcemic nephropathy

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Contributor Information and Disclosures

Author

Tibor Fulop, MD, Assistant Professor, Department of Internal Medicine, Division of Nephrology, University of Mississippi Medical Center
Tibor Fulop, MD is a member of the following medical societies: American College of Physicians and American Society of Diagnostic and Interventional Nephrology
Disclosure: Nothing to disclose.

Coauthor(s)

Mahendra Agraharkar, MD, MBBS, FACP, FASN, Clinical Associate Professor of Medicine, Baylor College of Medicine, President & CEO, Space City Associates of Nephrology
Mahendra Agraharkar, MD, MBBS, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Nephrology, and National Kidney Foundation
Disclosure: South Shore DaVita Dialysis Center  Ownership interest Other

Rupert Patel, MD, Physician, Division of Nephrology, Houston, Texas
Disclosure: Nothing to disclose.

Rajiv Gupta, MD, Assistant Professor, Department of Medicine, Texas A & M University Health Science Center; Consulting Staff, Veterans Affairs Medical Center
Rajiv Gupta, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Medical Editor

James W Lohr, MD, Fellowship Program Director, Professor, Department of Internal Medicine, Division of Nephrology, State University of New York at Buffalo
James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, 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, and Phi Beta Kappa
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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