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Dialysis disequilibrium syndrome: rapid recognition and rapid intervention decrease the risk of mortality a case study.

The Case

A 24-year-old female with a past history of poorly controlled insulin-dependent diabetes and lupus presented to the emergency room with weakness, anorexia, dyspnea, and general malaise. On physical assessment, bilateral lower extremity edema was noted, and crackles were present in the right base of the lungs. Blood chemistries showed an elevated creatinine (12.4mg/ dL), potassium (6.1mg/dL), BUN (185 mg/dL), and an estimated glomerular filtration rate (eGFR) of 10 mL/min/1.73 [m.sup.2]. Arterial blood gas results revealed a pH of 7.1, HC[O.sub.3] of 14, and C[O.sub.2] of 30, suggestive of metabolic acidosis. The patient was diagnosed with Stage 5 chronic kidney disease (CKD) or end stage renal disease (ESRD). Urgent hemodialysis was initiated using a bicarbonate dialysate and a single-use biocompatible membrane dialyzer (Optiflux[R] 160) with a blood flow rate of 250 mL/min and a dialysate flow rate of 800 mL/min. The ultrafiltration goal for fluid removal was set at 1.5 liters over two hours of treamaent time.

Approximately one hour and fifty minutes after starting the dialysis session, the patient became restless and complained of blurred vision, tremors, mild headache, nausea, and vomiting. Her blood pressure was 180/105, and her heart rate was 110. The patient was given promethazine (Phenergan[R]) 12.5 mg IV for nausea and clonidine 0.1 mg for hypertension per routine standing admission orders. Thirty minutes later, the patient developed generalized tonic-clonic convulsions, and the medical emergency team and physician were paged STAT. The dialysis session was terminated, and the patient was given lorazapam (Ativan[R]) intravenously. A STAT computed tomography (CT) scan and magnetic resonance image (MRI) revealed diffuse cerebral edema in the posterior perioccipital region. The patient was transferred to the neuro-intensive care unit (NICU), where the patient was lethargic and aroused to painful stimuli. Her pupils were 3 mm, equal, and sluggish to light bilaterally. The patient was confused and had a Glasco coma scale (GCS) score of 13. Mannitol was administered intravenously, and continuous renal replacement therapy (CRRT) was started a few hours later. CRRT is a gentler, 24-hour dialysis that uses a smaller kidney, lower blood flow, and slower ultrafiltration of excess fluid, solutes, and toxins.

Within 48 hours, the patient regained normal neurological function and had no further reports of adverse events. Blood chemistries showed a BUN of 40 mg/dL, creatinine of 2.5 mg/dL, and potassium of 4.2 mg/dL. Her blood gases revealed a pH of 7.42, C[O.sub.2] of 38, and HC[O.sub.3] of 22. CRRT was discontinued, and the patient was transferred to the renal medicine unit.


This patient experienced dialysis disequilibrium syndrome (DDS). DDS usually occurs in patients with acute renal failure who are starting dialysis for the first time when BUN levels are extremely high (Amato, Hlebovy, King, & Salai, 2008). Patients on chronic dialysis who are under-dialyzed are also susceptible (Amato et al., 2008). However, current advancements in renal replacement therapy (RRT) and the conservative management of patients through the various stages of CKD have allowed patients to start dialysis less often with very high BUN levels compared to several decades ago (Lopez-Almarez & Correa-Rotter, 2008). Although less common, early recognition and intervention are essential to decrease the potential deadly side effects of this disorder. This article discusses the pathophysiology, clinical manifestations, and treatment strategies to manage this potentially fatal syndrome. Nephrology nurses play a vital role in the prevention of DDS and in improving outcomes for patients with CKD who are on hemodialysis. Although some experts contend that DDS is a disorder of the past, the incidence and prevalence of DDS is unknown because it is often unrecognized and under-reported. Education and raising awareness of DDS is vital to saving lives.

Dialysis Disequilibrium Syndrome

First described in 1962 by Kennedy, Linton, and Eaton, DDS is an acute neurological dysfunction of hemodialysis with clinical manifestations of general malaise, mild headache, hypertension, nausea, vomiting, muscle cramps, tremors, blurred vision, seizures, convulsions, altered consciousness, coma, and in some cases, death (Patel, Delal, & Penesar, 2008). The symptoms are attributed to cerebral edema and usually present during or shortly after hemodialysis. DDS most often occurs during the first few dialysis treatments when patients are severely uremic and dialyzed aggressively (Attur, Kandavar, Kadavigere, & Baig, 2008). The term disequilibrium is used because the symptoms manifest as blood chemistries and fluid shift during hemodialysis (Patel et al., 2008).

The epidemiology of DDS is not well defined in the literature and is thought to be under-reported due to the wide range of clinical symptoms often attributed to other disorders (Bagshaw et al., 2004). Pediatric populations, the elderly, patients with underlying cerebral disorders, and patients with severe metabolic acidosis and extremely high BUN levels are at risk (Lopez-Alamarez & Correa-Rotter, 2008).


Although the pathophysiology of DDS is debated and not well understood, symptoms of DDS occur as water is shifted from the plasma into the brain during rapid hemodialysis, resulting in cerebral edema (Patel et al., 2008). In a steady condition, brain and plasma urea levels are similar (Patelet al., 2008). Differences in urea concentration between the plasma and the brain create an osmotic gradient between the two compartments (Patel et al., 2008). This concentration gradient influences the shift of fluid between the brain and the plasma. This shift is augmented during rapid hemodialysis therapy. Currently, three causal mechanisms are postulated for the development DDS: the reverse urea effect, intracellular organic osomolytes, and metabolic acidosis (Patel et al., 2008). However, debate remains as to the exact pathological processes responsible for the development of cerebral edema associated with DDS.

Reverse Urea Effect

With the reverse urea effect, high plasma urea levels are rapidly removed from blood during hemodialysis, creating an osmotic gradient between the brain and plasma. However, during this process, urea is removed more slowly across the blood-brain barrier than from the plasma. As plasma urea concentrations rapidly decrease and brain urea concentrations increase, a reverse osmotic gradient is created between the two compartments, which promotes water movement into the brain (Silver, Stems, & Halperin, 1996). The end result is cerebral edema.

One proposal for the delay in urea removal from the brain is down-regulation of the central nervous system (CNS) urea transporters (Hu, Bankir, Michelet, Rousselet, & Trinh-Trang-Tan, 2000). Because urea is a small molecule, it diffuses across the cell membrane very easily (Lopez-Almaraz & Correa-Rotter, 2008). However, during chronic uremic states, this shift may take hours to occur in the CNS. Brain cells adapt to chronic uremic states by decreasing the number of urea transporter cells, which ultimately results in slower or delayed diffusion of urea molecules (Patel et al. 2008).

Intracellular Organic Osmolytes

In addition to the reverse urea effect, experts theorize that organic osmolytes also play a role in the development of DDS. During high uremic states, osmolality in the extra-cellular fluid compartment is increased. To limit cerebral cellular dehydration, the body compensates by accumulating intracellular, organic osmolytes in the brain (Arieff, Massry, Barrientos, & Kleeman, 1973). During hemodialysis, as cerebral intracellular organic osmolytes are increased, a paradoxical effect occurs in which the cerebral intracellular pH is decreased, resulting in fluid accumulation in the brain or cerebral edema (Arieff, Guisade, Massry, & Lazarowitz, 1976; Trachtman, Futterweit, Tonidandel, & Gullans, 1993).

Metabolic Acidosis

Finally, some experts contend that correction of metabolic acidosis during hemodialysis may also contribute to the development of DDS (Patel et al., 2008). Metabolic acidosis is a common clinical manifestation of renal disease that occurs as a result of hydrogen ion accumulation in the plasma. Ideally, during CKD and metabolic acidosis, brain intracellular pH and cerebral spinal fluid pH remain normal (Patel et al., 2008). However, during hemodialysis, rapid correction of the plasma pH causes a paradoxical acidemia or decrease in the pH of the cerebral spinal fluid (Patel et al., 2008). The rapid attempt to attain hemostasis in blood pH results in a rapid increase in plasma bicarbonate concentration and arterial pH of the blood. To compensate for these changes, hypoventilation ensues, which increases plasma C[O.sub.2] levels. As plasma C[O.sub.2] levels increase, C[O.sub.2] diffuses quickly into the cerebrospinal fluid (CSF) (Patel et al., 2008). Further, diffusion of bicarbonate across the blood-brain barrier is delayed which further exacerbates CSF acidosis (Patel et al., 2008). These conditions are also associated with an increase in brain intracellular hydrogen ion concentration due to an increase in the production of organic acid in the brain. The increase in brain osmolyte concentration causes a 12% flux of water into the brain, leading to cerebral edema, which is the classic sign of DDS (Patel et al., 2008).

There is disagreement among experts that the reverse urea effect on organic osmolytes and the process of metabolic acidosis are the primary pathophysiological processes that lead to the development of DDS. A study was conducted by Chen et al. (2008) to evaluate whether interstitial or cytotoxic edema is responsible for the development of DDS. Eight patients with ESRD with BUN levels greater than 100 mg/dL were selected to participate in the study. Magnetic resonance (MR) images and clinical manifestations were observed before and after the first dialysis. MR imaging was used to measure the apparent diffusion coefficient, which sensitively measures and detects water dynamics at the tissue level. Results of the study strongly suggest that severe azotemia in patients with ESRD leads to interstitial brain edema, not cytotoxic brain edema as suggested by the reverse urea effect and organic osmolyte theories.

Clinical Manifestations Of DDS

Symptoms of DDS usually manifest as fatigue, mild headache, nausea, and vomiting, or can have more severe neurological manifestations, such as disturbed consciousness, convulsions, and coma. These symptoms are usually mild, transient, and self-limited; however, DDS can be fatal even though this is a rare occurrence (Patel et al., 2008). DDS occurs most commonly in the first few treatments of patients with ESRD who are newly started on hemodialysis, but can go undetected in patients with other comorbidities and can manifest at any point in the treatment regimen (Bagshaw et al., 2004).

Visual disturbances occurring in patients undergoing hemodialysis may also be a symptom of DDS. Im, Atabay, and Eller (2007) reported a case of a 38-year-old female with type 1 diabetes who presented with decreased visual acuity and bilateral optic nerve swelling associated with systemic signs and symptoms of DDS which included headaches, nausea, and papilledema. After renal transplantation, the patient had complete resolution of symptoms. They concluded that DDS should be suspected in patients with visual disturbances and focal neurological symptoms, and caution should be taken as to the possible risk of permanent visual impairment if this syndrome is not recognized.

Central nervous system complications may be a result of the multiple metabolic problems that occur with ESRD or can result from the dialysis procedure itself. Symptoms may begin with headache, nausea, vomiting, and/or hypotension, and usually occur during the latter portion or immediately after dialysis. If DDS is unrecognized or improperly treated, this symptomatology can progress to arrhythmias, seizures, coma, and death (Attur et al., 2008). Although it is commonly thought that patients only experience DDS during the first few treatments on hemodialysis, evidence has shown that for patients who are critically ill, septic, and on ventilator support, DDS can manifest after repeated sessions on hemodialysis. Shaikh, Loudon, and Hanssens (2010) described two cases of DDS occurring in patients with acute renal failure after more than one week on daily hemodialysis. Both patients were in septic shock but were stable on inotropic and ventilator support; however, both patients suffered neurological deterioration during a subsequent hemodialysis session, and emergency CT scan of the brain showed severe brain edema and herniation. Critically ill patients frequently require RRT or intermittent hemodialysis; therefore, it is imperative that healthcare providers participating in the care of these patients be aware of the signs and symptoms of DDS and remain vigilant in detecting this complication.

Management of DDS

Prevention is the most important factor in managing DDS. Because DDS occurs most often during or after the first dialysis treatment, several interventions can be implemented to prevent its occurrence. Although currently there are no evidence-based guidelines to prevent DDS, the most frequent method of prevention is a mild dialysis prescription using a low flux or less efficient dialyzer, lower blood flow rates (200 mL/min), and lower dialysate flow rates (500 mL/min), as well as shorter treatment time (two hours) (Patel et al., 2008). This allows for a slow, more sustained removal of urea and decreases the risk of developing cerebral edema (Bagshaw et al., 2004). The initial urea reduction ratio goal should be approximately 0.40 to 0.45 or a diffusive Kt/V goal of 0.6 to 0.7 (Patel et al., 2008).

Other methods used to prevent DDS are increasing the dialysate sodium or glucose concentration and using sodium profiling, but with varying results. Sodium profiling changes the sodium concentration of the dialysate fluid according to a time-dependent profile over the course of the dialysis session to avoid osmotic disequilibrium (Stiller, Bonnie-Schorn, Grassmann, Uhlenbusch-Korwer, & Mann, 2002). There have also been reports of the use of colloids, such as mannitol, which does not cross the blood-brain barrier, promotes cellular dehydration, and is often used to decrease or prevent cerebral edema (Adams & Koch, 2010; DiFresco, Landman, Jaber, & White, 2000). These interventions help to avoid major shifts of osmotic pressures and fluid during hemodialysis that can result in cerebral edema.


DDS is a complication that can be fatal. Because DDS is often undetected and under-reported, the epidemiology of DDS is not clearly defined in the literature. It most often occurs in patients with acute renal failure dialyzed for the first time when BUN concentrations are high. Although less likely, DDS can occur in patients receiving chronic hemodialysis therapy when they are under-dialyzed for various reasons, such as poor access flows and missing treatments (Amato et al., 2008). Those at greatest risk of developing DDS are the elderly, children, and patients with pre-existing neurologic complications, severe metabolic acidosis, and malignant hypertension (Amato et al., 2008). Although many experts contend that DDS is a disorder of the past, there are rare reports of fatalities due to the difficulty in reversing DDS when it has progressed in severity (Zepeda-Orozco & Quigley, 2012). Bagshaw et al. (2004) reported the case of a 22-year-old male patient with obstructive neuropathy and sepsis due to pneumonia who was started on hemodialysis and developed progressive neurological changes during the initial dialysis treatment. Shortly after the hemodialysis session, this patient had no pupillary reaction or brain stem reflexes. A CT scan showed diffuse cerebral edema, and he was declared brain dead (Bagshaw et al., 2004). Similarly, Shaikh and colleagues (2010) described two cases of DDS occurring in patients in the intensive care unit who were in septic shock and receiving ventilatory support. After more than one week on daily hemodialysis therapy, both patients suffered neurological deterioration. During a subsequent hemodialysis sessions, an emergent brain CT revealed severe brain edema and herniation.

While controversial, the fatal effects of DDS are thought to be attributable to several pathophysiological processes, such as the reverse urea effect, accumulation of organic osmolytes, and metabolic acidosis, which result in cerebral edema. Although there is no consensus regarding the exact pathophysiological pathway that leads to cerebral edema during hemodialysis, experts agree that cerebral edema is the primary characteristic of DDS.

Nephrology care providers should be cognizant of DDS and its deadly effects. Prevention is the major focus for managing DDS. Healthcare providers should be especially careful to monitor for signs and symptoms of DDS during the first dialysis treatment and shortly thereafter. However, DDS does not only occur for patients new to hemodialysis. It can also occur in patients who are receiving chronic hemodialysis therapy. Studies have identified patients with symptoms of DDS who have been receiving hemodialysis treatments for years. Nishizaki et al. (2012) reported the case of a patient who had been on dialysis for 10 years who failed to return for hemodialysis treatment for one week. Emergent hemodialysis was performed, and the patient developed DDS immediately after the hemodialysis treatment.

Strategies to prevent DDS include a slow dialysis treatment with a less efficient or low flux dialyzer, low blood flow and dialysate flow rates, and low ultrafiltration rates. Sodium modeling and the use of dialysate with high glucose and sodium concentration have also shown promise, but with varying results. Doorenbos, Bosma, and Lambert (2001) report the use of urea containing dialysate for a patient with diabetes, acute renal failure, and metformin toxicity, which was successful in preventing the progression DDS. Further, osmotic agents, such as IV mannitol, have also shown to be effective in preventing and treating DDS. DiFresco et al. (2000) reported the case of DDS in a 22-yearold female complicated by acute respiratory failure and mechanical ventilation successfully treated with hyperventilation and IV mannitol. According to Patel et al. (2008), a mannitol IV infusion of 1 g/kg/dialysis can be effective in the prevention of DDS during hemodialysis. Further, a combination of high-glucose dialysate and IV mannitol has also shown promise in the prevention of DDS (Rodrigo, Shideman, McHugh, Buselmeier, & Kjellstrand, 1977; Rosa, Shideman, McHugh, Duncan, & Kjellstrand, 1981).

No consensus on the epidemiology, pathophysiological processes, and management of DDS exists; thus, further research is needed. Research efforts should focus on the development of national evidence-based guidelines for the prevention and management of DDS. In addition, healthcare practitioners should be more proficient in diagnosing and reporting DDS.


DDS is a complication of hemodialysis that can occur during or immediately after the first hemodialysis treatment when urea levels are extremely high. It can also occur in any patient who receives hemodialysis (Zepeda-Orozco & Quigley, 2012); however, extreme uremia is not frequently observed in well-developed countries due to the early detection and conservative management of kidney disease and the advancements in RRT (Lopez-Almarez & Correa-Rotter, 2008). Therefore, DDS now occurs in fewer patients starting on dialysis when compared to several decades ago, and when it occurs, the symptoms are usually mild and self-limited (Lopez-Almarez & Correa-Rotter, 2008).

Although prevention is the most effective strategy to manage DDS, rapid recognition and intervention are essential to prevent or minimize the potential fatal complications of this disorder. Education of healthcare providers is essential to improve the quality of care provided to the renal population on hemodialysis. DDS is not a disease of the past. It is the responsibility of every nephrology care provider to be aware of this disorder and identify patients who are at risk so life-saving measures can be employed. Awareness and education are vital to improve quality care. Quality care is not an exception, but a right and an expectation that saves lives one person at a time.


To provide an overview of dialysis disequilibrium syndrome, its causes, and treatment modalities.


1. Define dialysis disequilibrium syndrome (DDS).

2. Identify the possible causes of DDS.

3. Explain the clinical manifestations of DDS.

4. Discuss treatment options for the treatment of patients who experience DDS.

This offering for 1.3 contact hours is provided by the American Nephrotogy Nurses' Association (ANNA).

American Nephrology Nurses' Association is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center Commission on Accreditation.

ANNA is a provider approved by the California Board of Registered Nursing, provider number CEP 00910.

Accreditation status does not imply endorsement by ANNA or ANCC of any commercial product.

This CNE article meets the Nephrology Nursing Certification Commission's (NNCC's) continuing nursing education requirements for certification and recertification.


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Stephanie Wrigkg DNP, MSN, MBA, RN, is a Nursing Instructor, Department of Physiological and Technological Nursing, Georgia-Regents University, Augusta, GA. She may be contacted directly via e-mail at

Jeanette Merriweather, DNP, RN, CNN, CNE, is an Assistant Professor, Department of Physiological and Technological Nursing, Georgia-Regents University, Augusta, GA.

Statement of Disclosure: The authors reported no actual or potential conflict of interest in relation to this continuing nursing education activity.

Note: Additional statements of disclosure and instructions for CNE evaluation can be found on page 338
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Title Annotation:Continuing Nursing Education
Author:Wright, Stephanie; Merriweather, Jeanette
Publication:Nephrology Nursing Journal
Article Type:Clinical report
Geographic Code:1USA
Date:Jul 1, 2013
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