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Phuong-Thu T. Pham1, Phuong-Mai T. Pham2, Parikh S1, Son V. Pham3, Phuong-Anh T. Pham4 and Phuong-Chi T. Pham5 1Department of Medicine, Nephrology Division, Kidney Transplant Program, David Geffen School of Medicine at UCLA 2Department of Medicine, Greater Los Angeles VA Medical Center and David Geffen School of Medicine at UCLA 3Department of Medicine, Cardiology Division, Bay Pines VA Medical Center, Bay Pines, Florida 4Department of Medicine, Division of Cardiovascular Diseases, VA Medical Center, University of Tennessee Health Science Center, Memphis, TN 5Department of Medicine, Nephrology Division, UCLA-Olive View Medical Center and David Geffen School of Medicine United States of America

New onset diabetes mellitus after transplantation (NODAT) is a serious and common complication following solid organ transplantation. NODAT has been reported to occur in 2% to 53% of all solid organ transplants. Kidney transplant recipients who develop NODAT have variably been reported to be at increased risk of fatal and nonfatal cardiovascular events and other adverse outcomes including infection, reduced patient survival, graft rejection, and accelerated graft loss compared with those who do not develop diabetes. Limited clinical studies in liver, heart, and lung transplants similarly suggested that NODAT has an adverse impact on patient and graft outcomes. Early detection and management of NODAT must, therefore, be integrated into the treatment of transplant recipients. Studies investigating the best predictive tool for identifying patients at risk for developing NODAT early after transplantation, however, are lacking. The clinical predictive values of fasting plasma glucose (FPG), oral glucose tolerance test (OGTT), and A1C in assessing the risk for the manifestation of NODAT are herein discussed.

Early post-transplant factors including delayed graft function (DGF), acute rejection episodes, nephrotoxic agents, post-transplant hypertension, dyslipidemia, and new onset diabetes mellitus after transplantation (NODAT) have all been implicated in worsening both short- and long-term morbidity and mortality after renal transplantation. Optimal management of the transplant recipient begins in the immediate postoperative period. This chapter provides a stepwise approach to the medical and urological management of the transplant recipient in the first 3 months after transplantation. The management of transplant recipients can be divided into three periods: immediate postoperative period, first week post-transplant, and first 3 months post-transplant. Immunosuppressive therapy is discussed in Chapter 9.

Recipients of nonrenal organ transplants including the liver, heart, and lung are at risk for developing acute kidney injury (AKI) and chronic kidney disease (CKD). Underlying hepatic or cardiopulmonary failure, prolonged intraoperative hemodynamic instability, and the use of calcineurin inhibitors and nephrotoxic medications have all been suggested to be contributory. The incidence of perioperative AKI has been reported to occur in 17% to 95% in liver transplant recipients, 5% to 30% in heart transplant recipients, and 5% to 60% in recipients of lung transplants. Among those who develop AKI, renal replacement therapy is required in 5% to 35%, 5% to 15%, and 8% to 10% in liver, heart, and lung transplant recipients, respectively. The current article presents an overview of the literature on the choice of dialysis modality and its associated advantages and disadvantages in the management of AKI after liver, heart, and lung transplants. Predictive factors for renal function recovery and the impact of AKI and CKD on survival will also be discussed.

Acute kidney injury (AKI) is common immediately after orthotopic liver transplantation (OLT), whereas chronic kidney disease (CKD) and end-stage renal disease (ESRD) increase in incidence with time. The cumulative risk of developing chronic renal failure post-OLT has been described to be approximately 8%, 14%, and 18% at 12, 36, and 60 months, respectively. Therefore identifying the risk factors for AKI or progressive CKD after OLT and developing strategies to either minimize the risks for AKI or retard the progression of CKD should be an integral part in the management of OLT recipients. Assessment of renal function pre- and post-OLT and an overview of the literature on the risk factors for early postoperative AKI and those affecting progressive CKD in long-term survivors are presented. Suggested therapeutic approaches to prevent, halt, or ameliorate renal dysfunction also are discussed.

This Practice Point commentary discusses the findings of a prospective study by Kuypers et al. that was designed to determine the best clinical diagnostic tool for identifying patients at risk of developing post-transplantation diabetes mellitus (PTDM) following renal transplantation. Fasting plasma glucose (FPG) levels on the day of transplantation and FPG levels and an oral glucose tolerance test (OGTT) at 5 days after transplantation were evaluated in de novo renal transplant recipients. The predictive values of these tests were assessed alongside other known risk factors for PTDM. A normal (vs diabetic) OGTT on day 5 was associated with a significantly reduced risk for PTDM (odds ratio 0.03; P = 0.0002). A similar reduction in the risk of PTDM was conferred by normal FPG levels on day 5 (odds ratio 0.06; P

Advances in immunosuppressive therapy and refinement in surgical techniques have allowed pancreas after kidney (PAK) transplantation to become a viable therapeutic option for patients with brittle type I diabetic recipients of a living donor or previous deceased kidney alone transplant. Although maintenance immunosuppressive therapy is not significantly changed after the addition of a pancreas, a temporary booster in immunosuppressive therapy and an increase in the dose of calcineurin inhibitor (CNI) are required after PAK transplantation. The latter has been implicated in the observed variable decline in kidney allograft function. We herein report two cases of kidney allograft dysfunction following PAK transplant due to biopsy-proven transplant, thrombotic microangiopathy (TMA). Whether PAK transplantation pre-disposes a subset of patients to the development of post-transplant TMA is not known. Diagnostic kidney biopsies should be considered in PAK transplant recipients with worsening kidney allograft function.

Renal transplantation is currently the preferred treatment modality for virtually all suitable candidates with end-stage renal disease. Compared with dialysis, kidney transplantation improves both patient survival and quality of life. Nonetheless, posttransplant cardiac complications are associated with increased morbidity and mortality after renal transplantation. When compared with the general population, cardiovascular mortality in transplant recipients is increased by nearly 10-fold among patients within the age range of 35 and 44 and at least doubled among those between the ages of 55 and 64. Although renal transplantation ameliorates cardiovascular disease risk factors by restoring renal function, it introduces new cardiovascular risks derived, in part, from immunosuppressive medications. We provide an overview of the literature on conventional and unconventional cardiovascular disease risk factors after renal transplantation, and discuss an approach to their medical management.

Studies of kidney function after orthotopic liver transplantation have yielded conflicting results, and there is a paucity of data on renal outcomes after combined liver–kidney transplantation. In this Review, authors from the University of California, Los Angeles attempt to synthesize the available findings into a cohesive update. Focus is given to the effect of the introduction of the MELD scoring system. Acute renal failure (ARF) is common immediately after orthotopic liver transplantation (OLT), whereas the incidences of chronic kidney disease (CKD) and end-stage renal disease increase with time. Introduction of the Model for End-stage Liver Disease (MELD) score—intended to prioritize patients with more-severe pretransplantation liver disease in general, and worse pretransplantation renal function in particular—for the allocation of liver grafts led to concerns about compromised patient and allograft survival and increased incidence of postoperative ARF and CKD. Nonetheless, it has been suggested that early OLT of candidates with baseline renal dysfunction improves post-transplantation renal outcomes. For OLT candidates with mild to moderate chronic renal impairment or recent-onset ARF, the decision of whether to perform OLT alone or combined liver–kidney transplantation (CLKT) can be challenging because no single factor has been shown to be predictive of the degree of renal function recovery or CKD progression following successful OLT. In this article, we provide an overview of the literature on renal function outcomes following OLT and CLKT, share our perspectives on the potential predictors of renal dysfunction or nonrecovery of renal function after OLT, and present United Network for Organ Sharing data on patient and allograft outcomes in CLKT recipients in the pre-MELD and post-MELD eras. Mechanisms that might underlie immunological protection of kidney grafts by liver allografts are also discussed.

The number of patients reinitiating dialysis after a failed transplant increases over time and has more than doubled between the year 1988 and 2010 (an increase from 2463 to 5588). More importantly, patients returning to dialysis have been shown to have a greater than three-fold increase in the annual adjusted mortality rates compared with those with a functioning graft. Continuation of immunosuppression to preserve residual graft function has been implicated to be a contributing factor, seemingly due to immunosuppression-associated cardiovascular and infectious complications and malignancy risk, among others. Nonetheless, maintenance low-dose immunosuppression has been suggested to confer survival benefit in patients returning to peritoneal dialysis. Whether early vs late reinitiation of dialysis or whether transplantectomy has an impact on patient survival remains poorly defined. Consensus guidelines for the management of a failed allograft are lacking. In this article, we present a literature overview on the ideal timing of dialysis reinitiation after graft loss, the management of immunosuppression after graft failure, and the risks and benefits of transplantectomy. The authors' perspectives on the management of this special patient population are also discussed.

The link between the nephrotic syndrome (NS) and malignancy was first described in 1922. In solid tumors, the NS is most often due to membranous glomerulonephropathy, whereas in common hematological malignancies, minimal-change disease predominates. Focal segmental glomerulosclerosis (FSGS) is among the least frequently reported renal lesion associated with malignancy. We report a case of the simultaneous diagnoses of FSGS and Hodgkin's lymphoma, and review the literature on various nephrotic glomerulonephropathies associated with common leukemia and lymphoma. Although nephrotic glomerulonephropathies rarely occur in association with acute leukemia, they have often been described in chronic lymphocytic leukemia (CLL). Membranoproliferative glomerulonephropathy and membranous glomerulonephropathy are the most common lesions observed in CLL. Nephrotic glomerulonephropathies have also been well documented among patients with lymphomas, in particular, Hodgkin's lymphoma. While minimal-change disease is most commonly found in association with Hodgkin's lymphoma, more diverse and complex renal lesions are associated with non-Hodgkin's lymphoma. FSGS remains a rare association with hematological malignancies. Nephrotic glomerulonephropathies are not only linked to solid-organ tumors, but also to hematolo-gical malignancies. A thorough evaluation, including a physical examination for lymphadenopathy and organomegaly, as well as a hematological evaluation, must be performed in all patients presenting with nephrotic glomerulonephropathies.

Hyponatremia is a common electrolyte disorder that frequently is overlooked and undertreated. Although the pathophysiological process of hyponatremia is complex, arginine vasopressin (AVP) is a common etiologic factor. Excess AVP release by osmotic or nonosmotic stimuli or both can lead to sodium and water imbalance. Conventional treatment options for hyponatremia, including water restriction and administration of sodium chloride with or without loop diuretics, do not directly address the underlying water retention induced by excess AVP in many cases. Clinical trials showed that AVP-receptor antagonists, including lixivaptan, tolvaptan, and conivaptan, produce aquaresis, the electrolyte-sparing excretion of free water, to correct serum sodium concentration. We review results from recent clinical trials involving AVP-receptor antagonists in the treatment of hyponatremia associated with AVP excess.

Aims: Hypomagnesemia has been implicated in adversely affecting diabetic complications. This is a retrospective study designed to determine whether there is any association between serum magnesium concentration [Mg 2+ ] and the rate of renal function deterioration, as determined by the slope of serum creatinine reciprocals versus time (1/SCr-vs-t), in patients with diabetes mellitus type 2 (DM2). Materials and methods: DM2 patients without known kidney disease seen at Olive View-UCLA Medical Center for any reason during January - March 2001 were included. For each patient, all available data from our electronic database for [Mg 2+ ], hemoglobin A 1C (HbA 1C ), serum creatinine (SCr), lipid profiles, routine urinary analysis, as well as history of hypertension and pharmacy profiles were retrieved. The average of all parameters obtained and linear regression analyses for the slope of 1/SCr-vs-t plot were performed for each patient. Patients were stratified by gender and divided into four groups based on increasing [Mg 2+ ]. Correlations between each parameter including the slope of 1/SCr-vs-t and the four magnesium groups were analyzed. Results: 252 males and 298 females with a mean follow-up of 62.6 ± 22.5 months were included. Patients belonging to lower [Mg 2+ ] groups for both genders had significantly worse slopes of 1/SCr-vs-t plot independent of the presence of hypertension and use of ACEI/ARB, diuretics, HMG-CoA enzyme inhibitors or aspirin. In a multivariate regression analysis controlling for age, HbA 1C and various components of the lipid profile, [Mg 2+ ] remained an independent predictor for the slope of 1/SCr-vs-t. A trend for worse proteinuria based on routine urinary analysis was observed among patients belonging to the lowest [Mg 2+ ] group. Conclusions: Lower [Mg 2+ ] is associated with a faster renal function deterioration rate in DM2 patients.

Background Thrombotic microangiopathy (TMA) is a well-known complication after renal allograft transplantation. In most cases, calcineurin inhibitor is believed to play a role in the development of this disorder. Recent studies have shown that a deficiency in the activity of the von Willebrand factor-cleaving metalloprotease ADAMTS13 causes thrombotic thrombocytopenic purpura. A similar mechanism occurring in patients who develop TMA after renal transplantation has not been described. Methods Analysis of plasma samples from a patient who developed TMA after receiving a cadaveric renal allograft revealed undetectable ADAMTS13 activity and the presence of its inhibitors. Results Discontinuation of cyclosporine and daily plasma exchange increased the ADAMTS13 activity, which was followed by resolution of the microangiopathic hemolysis and improvement of the graft function. At 3-month follow-up, the ADAMTS13 activity remained in the normal range and no inhibitors were detected. Conclusions This is the first case to demonstrate a correlation between the presence of ADAMTS13 inhibitors and transplant-associated TMA. Autoimmune inhibitors of ADAMTS13 should be considered in patients with transplant-associated thrombotic microangiopathy. The role of calcineurin inhibitor in the formation of autoantibodies to ADAMTS13 remains to be explored.

The development of thrombotic microangiopathy (TMA) associated with the use of cyclosporine has been well documented. Treatments have included discontinuation or reduction of cyclosporine dose with or without concurrent plasma exchange, plasma infusion, anticoagulation, and intravenous immunoglobulin G infusion. However, for recipients of organ transplantation, removing the inciting agent is not without the attendant risk of precipitating acute rejection and graft loss. The last decade has seen the emergence of tacrolimus as a potent immunosuppressive agent with mechanisms of action virtually identical to those of cyclosporine. As a result, switching to tacrolimus has been reported to be a viable therapeutic option in the setting of cyclosporine-induced TMA. With the more widespread application of tacrolimus in organ transplantation, tacrolimus-associated TMA has also been recognized. However, literature regarding the incidence of the recurrence of TMA in patients exposed sequentially to cyclosporine and tacrolimus is limited. We report a case of a living donor renal transplant recipient who developed cyclosporine-induced TMA that responded to the withdrawal of cyclosporine in conjunction with plasmapheresis and fresh frozen plasma replacement therapy. Introduction of tacrolimus as an alternative immunosuppressive agent resulted in the recurrence of TMA and the subsequent loss of the renal allograft. Patients who are switched from cyclosporine to tacrolimus or vice versa should be closely monitored for the signs and symptoms of recurrent TMA.

Predicted sodium concentrations [Na(+)] based on traditional calculations for the correction of hyponatremia often do not match treated [Na(+)], for various reasons. In many situations, hyponatremia is corrected at unexpectedly rapid rates. The authors present an analysis of two cases of overly rapid correction of hyponatremia despite apparently appropriate management based on initial evaluations. The mistakes involved are discussed and simple calculations demonstrated to prove that the overcorrections did not occur at random. Overcorrection in one case involved miscommunications between the emergency room and admitting physicians regarding the amount of saline and potassium already administered to the patient. Unexpected hypoosmotic polyuria was responsible for overcorrection in the other case. Overcorrection of hyponatremia may be preventable in many cases. In general, overcorrection of hyponatremia is caused by either "too much salt (Na(+) + K(+)) gained" or "too much water lost." Recognizing common pitfalls will enable physicians to avoid overcorrection and its attendant risk of fatal osmotic demyelinating syndrome (ODS).

The advent of potent antiplatelet and antithrombotic agents over the past decade has resulted in significant improvement in reducing ischemic events in acute coronary syndrome (ACS). However, the use of antiplatelet and antithrombotic combination therapy, often in the settings of percutaneous coronary intervention (PCI), has led to an increase in the risk of bleeding. In patients with non-ST elevation myocardial infarction treated with antithrombotic agents, bleeding has been reported to occur in 0.4%-10% of patients, whereas in patients undergoing PCI, periprocedural bleeding occurs in 2.2%-14% of cases. Until recently, bleeding was considered an intrinsic risk of antithrombotic therapy, and efforts to reduce bleeding have received little attention. There have been increasing data demonstrating that bleeding is associated with adverse outcomes, including myocardial infarction, stroke, and death. Therefore, it is imperative to optimize patient outcomes by adopting pharmacological and nonpharmacological strategies to minimize bleeding while maximizing treatment efficacy. In this paper, we present a review of the bleeding classifications used in large-scale clinical trials in patients with ACS and those undergoing PCI treated with antiplatelets and antithrombotic agents, adverse outcomes, particularly mortality associated with bleeding complications, and suggested predictive risk factors. Potential mechanisms of the association between bleeding and mortality and strategies to reduce bleeding complications are also discussed.

Although renal transplantation ameliorates cardiovascular risk factors by restoring renal function, it introduces new cardiovascular risks including impaired glucose tolerance or diabetes mellitus, hypertension, and dyslipidemia that are derived, in part, from immunosuppressive medications such as calcineurin inhibitors, corticosteroids, or mammalian target of rapamycin inhibitors. New onset diabetes mellitus after transplantation (NODAT) is a serious and common complication following solid organ transplantation. NODAT has been reported to occur in 2% to 53% of all solid organ transplants. Kidney transplant recipients who develop NODAT have variably been reported to be at increased risk of fatal and nonfatal cardiovascular events and other adverse outcomes including infection, reduced patient survival, graft rejection, and accelerated graft loss compared with those who do not develop diabetes. Identification of high-risk patients and implementation of measures to reduce the development of NODAT may improve long-term patient and graft outcome. The following article presents an overview of the literature on the current diagnostic criteria for NODAT, its incidence after solid organ transplantation, suggested risk factors and potential pathogenic mechanisms. The impact of NODAT on patient and allograft outcomes and suggested guidelines for early identification and management of NODAT will also be discussed.

Over the past decade ABO incompatible transplantation has emerged as an important potential source for increasing living kidney transplantation in selected transplant centers. Early reports suggest that patients who have elevated serum anti-blood group antibody titers (anti-A/B) before transplantation and a rebound antibody production after antibody removal may be at high immunological risk. With currently available immune modulation protocols and immunosuppressive therapy, excellent short- and long-term patient and graft survival rates have been achieved even in those with high anti-A/B antibody titers before plasmapheresis or immunoadsorption. Nonetheless, acute infection with an organism possessing surface markers analogous to blood group antigens such as carbohydrate structures on the surface of bacterial cell wall occurring before the firm establishment of accommodation can trigger the onset of acute antibody-mediated rejection. We herein report a case of delayed hyperacute rejection in an A1 to O, ABO incompatible transplant recipient following an episode of Clostridium difficile infection.

In patients undergoing percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS), both periprocedural acute myocardial infarction and bleeding complications have been shown to be associated with early and late mortality. Current standard antithrombotic therapy after coronary stent implantation consists of lifelong aspirin and clopidogrel for a variable period depending in part on the stent type. Despite its well-established efficacy in reducing cardiac-related death, myocardial infarction, and stroke, dual antiplatelet therapy with aspirin and clopidogrel is not without shortcomings. While clopidogrel may be of little beneficial effect if administered immediately prior to PCI and may even increase major bleeding risk if coronary artery bypass grafting is anticipated, early discontinuation of the drug may result in insufficient antiplatelet coverage with thrombotic complications. Optimal and rapid inhibition of platelet activity to suppress ischemic and thrombotic events while minimizing bleeding complications is an important therapeutic goal in the management of patients undergoing percutaneous coronary intervention. In this article we present an overview of the literature on clinical trials evaluating the different aspects of antithrombotic therapy in patients undergoing PCI and discuss the emerging role of these agents in the contemporary era of early invasive coronary intervention. Clinical trial acronyms and their full names are provided in Table 1.

Phuong-Thu T Pham1, Gerald S Lipshutz2, Phuong-Truc T Pham3, Joseph Kawahji1, Jennifer S Singer4, Phuong-Chi T Pham51Division of Nephrology, Department of Medicine, Kidney and Pancreas Transplant Program, University of California at Los Angeles, David Geffen School of Medicine, Los Angeles, California; 2Kidney and Pancreas Transplant Program, Department of Surgery and Urology, University of California at Los Angeles, David Geffen School of Medicine, Los Angeles, California; 3Department of Science, Penn State University, Worthington-Scranton, Dunmore, Pennsylvania; 4Renal Transplantation and Pediatric Urology, Department of Urology, University of California at Los Angeles, David Geffen School of Medicine, Los Angeles, California; 5Division of Nephrology, Department of Medicine, University of California at Los Angeles, David Geffen School of Medicine, Los Angeles, and Olive-View-UCLA Medical Center, Sylmar, California, USAAbstract: The introduction of new immunosuppressive agents into clinical transplantation in the 1990s has resulted in excellent short-term graft survival. Nonetheless, extended long-term graft outcomes have not been achieved due in part to the nephrotoxic effects of calcineurin inhibitors (CNIs) and the adverse effects of steroid on cardiovascular disease risk factors. Induction therapy with lymphocyte depleting antibodies has originally been introduced into renal transplantation to provide intense immunosuppression in the early post-transplant period to prevent allograft rejection. Over the past half decade, induction therapy with both non-lymphocyte depleting (basiliximab and daclizumab) and lymphocyte-depleting antibodies (antithymocyte antibodies, OKT3, alemtuzumab) has increasingly been utilized in steroid or CNI sparing protocols in the early postoperative period. Alemtuzumab is a humanized monoclonal antibody targeted against CD52 on the surface of circulatory mononuclear cells. The ability of alemtuzumab (Campath-1H) to provide rapid and profound depletion of lymphocytes from the peripheral blood has sparked interest in the use of this agent as induction therapy in steroid and/or CNI minimization or avoidance protocols. This article provides an overview of the literarure on the evolving role of alemtuzumab in renal transplantation.Keywords: alemtuzumab, Campath-1H, induction, renal transplantation, calcineurin inhibitor minimization, steroid avoidance

Phuong-Thu T. Pham, Phuong-Chi T. Pham, REFERENCES and Alan H. Wilkinson Los Angeles, California 1. Ruggenenti P: Post-transplant hemolytic-uremic syndrome. Kidney Int 62:1093–1104, 2002 Correspondence to Phuong-Thu T. Pham, M.D., Nephrology Divi2. Crespo M, Pascual M, Tolkoff-Rubin N, et al: Acute humoral sion, Kidney and Pancreas Transplantation, Department of Medicine, rejection in renal allograft recipients: I. Incidence, serology and University of California at Los Angeles School of Medicine, 200 UCLA clinical characteristics. Transplantation 71:652–658, 2001 Medical Plaza, Suite 365C, Los Angeles, CA 90024. 3. Montgomery R, Zachary A, Racusen L, et al: Plasmapheresis and E-mail: pctp@ucla.edu intravenous immune globulin provides effective rescue therapy for refractory humoral rejection and allows kidneys to be successfully transplanted into cross-match-positive recipients. Transplantation REFERENCES 70:887–895, 2000 1. Tsai HM, Lian EC-Y: Antibodies to von Willebrand factor-cleaving 4. Pascual M, Saidman S, Tolkoff-Rubin N, et al: Plasma exchange protease in acute thrombotic thrombocytopenic purpura. N Engl J and tacrolimus-mycophenolate rescue for acute humoral rejection Med 26:1585–1594, 1998 in kidney transplantation. Transplantation 66:1460–1464, 1998 2. Furlan M, Robbles R, Galbusera M, et al: Von Willebrand factorcleaving protease in thrombotic thrombocytopenic purpura and the hemolytic-uremic syndrome. N Engl J Med 26:1578–1584, 1998 3. Pham PT, Danovitch GM, Wilkinson AH, et al: Inhibitors of Thrombotic microangiopathy ADAMTS-13: A potential factor in the cause of thrombotic microangiopathy in a renal allograft recipient. Transplantation 74:1077– following organ transplantation 1080, 2002 4. Ruggenenti P: Post-transplant hemolytic-uremic syndrome. Kidney Int 62:1093–1104, 2002

Sheehan's syndrome has been attributed to ischemic damage of the pituitary gland or hypothalamic-pituitary stalk during the peripartum period. Well-described clinical features of Sheehan's syndrome include hypothyroidism, adrenal insufficiency, hypogonadism, growth hormone deficiency, hypoprolactinemia, and different sodium and water disturbances. The occurrence of sodium and water disturbances associated with Sheehan's syndrome depends on the degree of pituitary damage, time of onset since the initial pituitary insult, and concurrent medical conditions that also may play a role in sodium and water balance. We present a patient with Sheehan's syndrome with severe chronic hyponatremia; discuss a potential problem in the patient's management; and review the literature for various sodium and water disturbances, including acute and chronic hyponatremia as well as overt and subclinical central diabetes insipidus. Although Sheehan's syndrome is more prevalent in developing countries, the increasingly large immigrant population within the United States warrants better awareness of this syndrome and its potential complicating sodium and water disturbances. Prompt diagnosis and an understanding of the pathogenic mechanisms of sodium and water disturbances associated with Sheehan's syndrome may avoid potential treatment-related complications.