Body composition and heart rate variability to achieve dry weight and tolerance.

Autonomic dysfunction in patients with end- stage renal disease is associated with poor prognosis. Heart rate variability (HRV), determined by the standard deviation of the normal R- R interval, has been reported to be a useful evaluation of cardiac autonomic modulation. The relationship between HRV and hydration status (HS) can be analyzed by whole body bioimpedance spectroscopy. This allows a classification of patients according the combination of HS with predialysis systolic blood pressure. Differences in HRV can be studied in patients with high over hydration, but normal or low blood pressure, with respect to fluid-overloaded/hypertensive patients and normohydrated/normotensive patients. In conclusion, the assessment of the autonomic nervous system response to the hemodialysis treatment in end- stage renal disease patients, classified according to a reliable and quantitative measurement of their fluid overload, could permit better management of both arterial blood pressure and HS.

Prospective multicenter study on epidemiology of acute kidney injury in the ICU: a critical care nephrology Italian collaborative effort (NEFROINT).

Acute kidney injury (AKI) is an independent risk factor for mortality in critically ill patients whose epidemiology has been made unclear in the past by the use of different definitions across various studies. The RIFLE consensus definition has provided a unifying definition for AKI leading to large retrospective studies in different countries. The present study is a prospective observational multicenter study designed to prospectively evaluate all incident admissions in 10 Intensive Care Units (ICUs) in Italy and the relevant epidemiology of AKI. A simple user-friendly web-based data collection tool was created with the scope to serve for this study and to facilitate future multicenter collaborative efforts. We enrolled 601 consecutive patients into the study; 25 patients with End-Stage Renal Disease were excluded leaving 576 patients for analysis. The median age was 66 (IQR 53-76) years, 59.4% were male, while median SAPS II and APACHE II scores were 43 (IQR 35-54) and 18 (IQR 13-24), respectively. The most common diagnostic categories for ICU admission were: respiratory (27.4%), followed by neurologic (17%), trauma (14.4%), and cardiovascular (12.1%). Crude ICU and hospital mortality were 21.7% and median ICU length of stay was 5 days (IQR 3, 14). Of 576 patients, 246 patients (42.7%) had AKI within 24 hours of ICU admission while 133 developed new AKI later during their ICU stay. RIFLE-initial class was Risk in 205 patients (54.1%), Injury in 99 (26.1%) and Failure in 75 (19.8%). Progression of AKI to a worse RIFLE class was seen in 114 patients (30.8% of AKI patients). AKI patients were older, with higher frequency of common risk factors. 116 AKI patients (30.6%) fulfilled criteria for sepsis during their ICU stay, compared to 33 (16.7%) of non-AKI patients (P<0.001). 48 patients (8.3%) were treated with renal replacement therapy (RRT) in the ICU. Patients were started on RRT a median of 2 (IQR 0-6) days after ICU admission. Among AKI patients, they were started on RRT a median of 1 (IQR 0-4) days after fulfilling criteria for AKI. Median duration of RRT was 5 (IQR 2-10) day. AKI patients had a higher crude ICU mortality (28.8% vs. non-AKI 8.1%, P<0.001) and longer ICU length of stay (median 7 days vs. 3 days [non-AKI], P<0.001). Crude ICU mortality and ICU length of stay increased with greater severity of AKI. Two hundred twenty five patients (59.4% of AKI patients) had complete recovery of renal function, with a SCr at time of ICU discharge which was ≤120% of baseline; an additional 51 AKI patients (13.5%) had partial renal recovery, while 103 (27.2%) had not recovered renal function at the time of death or ICU discharge. Septic patients had more severe AKI, and were more likely to receive RRT with less frequency of renal function recovery. Patients with sepsis had higher ICU mortality and longer ICU stay. The study confirms previous analyses describing RIFLE as an optimal classification system to stage AKI severity. AKI is indeed a deadly complication for ICU patients where the level of severity correlated with mortality and length of stay. The tool developed for data collection resulted user friendly and easy to implement. Some of its features including a RIFLE class alert system, may help the treating physician to collect systematically AKI data in the ICU and possibly may guide specific decision on the institution of renal replacement therapy.

Comparison of estimated glomerular filtration rate (eGFR) using the MDRD and CKD-EPI equations for CKD screening in a large population.

BACKGROUND/AIMS: recently, the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) proposed a new equation for estimating glomerular filtration rate (eGFR), which could potentially replace the Modified Diet for Renal Disease Study (MDRD) equation in routine clinical use. Our aim was to evaluate the correlation between them and to compare the prevalence of each CKD stage using these two equations. METHODS: we measured serum creatinine in 38,188 consecutive patients and calculated eGFR using the CKD-EPI and MDRD equations. We also compared the distribution of CKD stages for both equations. RESULTS: there was very good correlation between eGFR estimated by CKD-EPI and MDRD at values < 60 ml/min × 1.73 m2, but not at higher values. Estimated prevalence of CKD (eGFR < 60 ml/min × 1.73 m2) was 5.9% with CKD-EPI and 7.5% with MDRD. Furthermore, the prevalence of CKD Stage 2 was lower with CKD-EPI (33.8% vs. 49.1%. with MDRD). CONCLUSION: the use of the CKD-EPI equation results in a lower estimated prevalence of CKD, compared to the MDRD equation. This may have important implications for public health and clinical practice, as well as for future modification of guidelines for laboratories.

ADQI 7: the clinical management of the Cardio-Renal syndromes: work group statements from the 7th ADQI consensus conference.

Many patients with heart failure have underlying renal dysfunction, and similarly, patients with kidney failure are prone to cardiac failure. This has led to the concept of cardio-renal syndromes, which can be an acute or chronic cardio-renal syndrome, when cardiac failure causes deterioration in renal function, or acute and/or chronic Reno-Cardiac syndrome, when renal dysfunction leads to cardiac failure. Patients who develop these syndromes have increased risk of hospital admission and mortality. Although there are clinical guidelines for managing both heart failure and chronic kidney disease, there are no agreed guidelines for managing patients with cardio-renal and/or Reno-Cardiac syndromes, as these patients have typically been excluded from clinical trials. We have therefore reviewed the currently available published literature to outline a consensus of current best clinical practice for these patients.

Clinical pattern of adult polycystic kidney disease in a northeastern region of Italy.

BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic renal disorder, with a prevalence of 1 : 500 to 1 : 1,000. ADPKD is genetically heterogeneous: the genes involved are PKD1 and PKD2. ADPKD occurs worldwide and in all ethnic groups and is an important cause of CKD Stage 5. Prevalence of ADPKD on renal replacement therapy (RRT) in Italy has been reported to be 8.2%. In the dialysis population of Vicenza, a province in Northeastern Italy, it accounts for 13.4%. The study aims to investigate reasons for the high prevalence of ADPKD in our region and to describe the clinical profile and genetics of these patients. METHODS: Since April 2007, ADPKD patients have been enrolled. Patients from families not native to Vicenza have been excluded. The diagnosis of ADPKD is defined by ultrasound criteria. Complete clinical details have been recorded, including family history. We have used linkage analysis to identify the gene involved in each family. RESULTS: We describe the first 100 patients recruited from a total of 42 families. 29 patients were in ESRD at the time of enrollment. Renal stones and hepatic cysts were present in 24% and 40%, respectively. The majority of the ADPKD patients (61%) were diagnosed either incidentally or by screening. Positive family history was recorded in 86 patients. The involved gene was PKD1 in 83.7% and PKD2 in 16.3% of the studied patients. PKD2 patients presented the common haplotype. CONCLUSIONS: It is the first epidemiological study from Northeastern Italy reporting clinical profile and genetic analysis of ADPKD patients. The clinical profile of the patients is similar to previous reports, but there is a high prevalence of ADPKD in our region. The presence of a common haplotype is in accordance with our hypothesis of a founder effect in our province, suggesting that a strong lineage-specific gene is present. If the sequence analysis confirms the same mutation, this might suggest a common ancestral origin and a segregation of a specific mutation.

The role of extracorporeal blood purification therapies in the prevention of radiocontrast-induced nephropathy.

Radiocontrast-induced nephropathy (RCIN) is a common and potentially serious complication following diagnostic and therapeutic cardiology procedures using radiocontrast media. The first and most important step in reducing the likelihood of RCIN is to identify patients at risk, by medical history and measurement of serum creatinine concentration to allow calculation of estimated glomerular filtration rate (GFR). Extracorporeal blood purification effectively removes radiocontrast media from the circulation. Periprocedural extracorporeal blood purification (hemodialysis or continuous renal replacement therapy) does not reduce the incidence of RCIN compared with standard medical therapy, and cannot be recommended at this time. The potential benefit of continuous venovenous hemofiltration published by a single center should be confirmed with further studies before it can be recommended or disregarded, and higher doses of continuous renal replacement therapy may also merit further investigation.

Effect of vitamin E-coated dialysis membranes on anemia in patients with chronic kidney disease: an Italian multicenter study.

BACKGROUND: Increased oxidant stress is increasingly recognized as a crucial factor in anemia in patients with chronic kidney disease. Vitamin E-coated membranes (VECMs) consist of a multilayer membrane with liposoluble vitamin E on the blood surface allowing direct free radical scavenging at the membrane site, which is of potential clinical benefit. Our objective was to examine the effect of VECMs on anemia in chronic hemodialysis (HD). METHODS: We enrolled 172 stable chronic HD patients (94 men, 78 women, age 65.4 +/- 13.4 years) in an open-label multicenter study. They were shifted from their previous dialyzer to VECM for 1 year. Hemoglobin (Hb) levels and recombinant human erythropoietin (rHuEpo) dosage were analyzed after 4, 8, and 12 months on the VECM and compared with baseline values using paired tests. RESULTS: Hb significantly increased from 10.9 +/- 1.2 g/dL at baseline to 11.7 +/- 1.2 g/dL after 12 months (p<0.001) on VECMs. Conversely, the rHuEpo dosage decreased from 7,762 +/- 5,865 IU/week at baseline to 6,390 +/- 5,679 IU/week after 12 months (p<0.001). The proportion of patients who were at target Hb levels (European Best Practice Guidelines) increased from 49.4% at baseline to 80% after 12 months (p<0.001). CONCLUSIONS: Dialysis with VECM in stable chronic HD patients was associated with significantly improved Hb levels and lower rHuEpo requirements. These results suggest that the antioxidant properties of VECMs may impact favorably on anemia management in chronic HD patients. Possible mechanisms include enhanced membrane biocompatibility, reduced oxidative stress and inflammation with VECMs, resulting in improved red blood cell survival and/or rHuEpo responsiveness. This therapy may potentially contribute to more effective anemia management in hemodialysis patients, and merits further rigorous study.

The epidemiology of cardiac surgery-associated acute kidney injury.

PURPOSE: To describe current knowledge on the epidemiology of cardiac surgery-associated acute kidney injury (CSA-AKI) and to formulate recommendations for clinical practice and a research agenda. METHODS: After a modified Delphi analysis by the Acute Dialysis Quality Initiative (ADQI), 4 questions on the epidemiology of CSA-AKI and recommendations for clinical practice and a research agenda were formulated and addressed. RESULTS: Existing studies on CSA-AKI use over 35 different definitions for CSA-AKI. In addition, there may be important differences in patient characteristics and procedures. This explains the significant variations in reported incidence. Most studies report on CSA-AKI as defined by the need for renal replacement therapy. However, even small decreases in kidney function are associated with a worsened outcome. The workgroup formulated the recommendation to use the AKIN consensus criteria for AKI. One should differentiate early CSA-AKI, caused by the procedure, and late CSA-AKI, associated with the procedure. There may be different clinical scenarios: acute on chronic CSA-AKI, AKI prior to CS, and AKI occurring post CS. Risk factors should be differentiated between pre-, intra-, and post-CS, and between patient-, process-, and procedure-related. Endpoints should include both short-term and long-term outcomes. CONCLUSIONS: Existing data on the epidemiology of CSA-AKI are difficult to compare due to variations in definition and patient cohort. A modified Delphi analysis resulted in a series of recommendations for future research on CSA-AKI.

Genotype/phenotype observations in African Americans with Bartter syndrome.

BACKGROUND: Two Bartter syndrome phenotypes have been described, and molecular analyses demonstrate mutations in 1 of 3 genes encoding ascending limb of Henle transporters. We report phenotypic observations in 5 African American children with Bartter syndrome in the context of a distinct genotype. METHODS: Mutation analyses were performed in 5 unrelated African American children with Bartter syndrome. These results were correlated to clinical and laboratory data. Calcium metabolism was evaluated with a bone disk bioassay. RESULTS: Mutation analyses demonstrated homozygous deletion of the ClC-Kb gene in all children. Two children had polyhydramnios and premature birth; the others were born at term and presented with failure to thrive or dehydration. All receive indomethacin, spironolactone, and potassium chloride with improved but borderline hypokalemia. Growth has improved with therapy, but height SD scores range from -3.9- to -1.4. Urinary calcium excretion is normal, and bone disk bioassay shows no abnormal calciotropic activity. No patient had nephrocalcinosis, but renal sonograms show loss of corticomedullary differentiation. CONCLUSIONS: African Americans with Bartter syndrome genotyped to date have homozygous deletion of ClC-Kb Clinical observations in our patients include partial correction of hypokalemia and suboptimal growth despite therapy. Abnormal calciotropic activity and nephrocalcinosis are not seen, but renal ultrasounds are abnormal.

Parameters of high bone-turnover predict bone loss in renal transplant patients: a longitudinal study.

BACKGROUND: Osteoporosis is a serious complication of kidney transplantation. Various factors have been postulated to contribute to posttransplant bone loss, among them treatment with corticosteroids, the use of cyclosporine and cyclosporine-like agents, and persistent hyperparathyroidism. In a previous cross-sectional study of long-term renal transplant recipients, we observed that osteoporosis or osteopenia was present in 88% of patients. Because biochemical markers of bone formation (serum osteocalcin) and bone resorption (urine pyridinoline, PYD, and deoxypyridinoline, DPD) were elevated in the majority of study subjects, we hypothesized that elevated rates of bone-turnover contribute to posttransplant bone loss in long-term renal transplant patients. This study was performed to examine this hypothesis. METHODS: The study population was composed of 62 patients who were more than 1-year postrenal transplantation and who had preserved renal function. They were followed prospectively for 1 year. Biochemical markers of bone-turnover were measured at study entry, and patients were classified as having high bone-turnover based on elevated urinary levels of at least one marker of bone resorption (i.e., PYD or DPD) and/or serum osteocalcin (group 1). If none of these were present, they were classified as having normal bone-turnover (group 2). Bone mineral density (BMD) was measured by dual energy x-ray absorptiometry (DEXA) at time of entry into the study and again after 1 year of follow-up. The changes in BMD at the lumbar spine, hip, and wrist over the period of the study were compared between the high and normal bone-turnover groups. RESULTS: Forty-three patients (69%) were classified as having high bone-turnover (Group 1), and 19 patients (31%) were classified as having normal bone-turnover (Group 2). There was a statistically significant difference in change in BMD between the two groups at the lumbar spine (-1.11+/-0.42%, high bone-turnover, vs. 0.64+/-0.54%, normal bone-turnover; P=0.02) and the hip (-0.69+/-0.38%, high bone-turnover, vs. 1.36+/-0.66%, normal bone-turnover; P=0.006). Whereas group 2 had stable bone mass, group 1 exhibited bone loss at these skeletal sites. CONCLUSIONS: Our results indicate that bone loss is greater in renal transplant recipients with elevated biochemical markers of bone-turnover, suggesting that these markers may be useful in identifying patients at risk for continued bone loss. These data support the hypothesis that continued bone loss in long-term renal transplant recipients is associated with high bone-turnover. If accelerated bone resorption does play a role in posttransplant bone loss, this would provide a strong rationale for use of antiresorptive therapy for the prevention and treatment of this complication.

Mutations in the Na-Cl cotransporter reduce blood pressure in humans.

The relationship between salt homeostasis and blood pressure has remained difficult to establish from epidemiological studies of the general population. Recently, mendelian forms of hypertension have demonstrated that mutations that increase renal salt balance lead to higher blood pressure, suggesting that mutations that decrease the net salt balance might have the converse effect. Gitelman's syndrome, caused by loss of function mutations in the Na-Cl cotransporter of the distal convoluted tubule (NCCT), features inherited hypokalemic alkalosis with so-called "normal" blood pressure. We hypothesized that the mild salt wasting of Gitelman's syndrome results in reduced blood pressure and protection from hypertension. We have formally addressed this question through the study of 199 members of a large Amish kindred with Gitelman's syndrome. Through genetic testing, family members were identified as inheriting 0 (n=60), 1 (n=113), or 2 (n=26) mutations in NCCT, permitting an unbiased assessment of the clinical consequences of inheriting these mutations by comparison of the phenotypes of relatives with contrasting genotypes. The results demonstrate high penetrance of hypokalemic alkalosis, hypomagnesemia, and hypocalciuria in patients inheriting 2 mutant NCCT alleles. In addition, the NCCT genotype was a significant predictor of blood pressure, with homozygous mutant family members having significantly lower age- and gender-adjusted systolic and diastolic blood pressures than those of their wild-type relatives. Moreover, both homozygote and heterozygote subjects had significantly higher 24-hour urinary Na(+) than did wild-type subjects, reflecting a self-selected higher salt intake. Finally, heterozygous children, but not adults, had significantly lower blood pressures than those of the wild-type relatives. These findings provide formal demonstration that inherited mutations that impair renal salt handling lower blood pressure in humans.

Gitelman's syndrome revisited: an evaluation of symptoms and health-related quality of life.

BACKGROUND: Gitelman's syndrome (GS), also called Gitelman's variant of Bartter's syndrome, is an autosomal recessive renal disorder characterized by hypokalemia, hypomagnesemia, metabolic alkalosis, and hypocalciuria. GS is caused by inactivating mutations in the thiazide-sensitive sodium chloride cotransporter gene (NCCT). It is also known as the "milder" form of Bartter's syndrome, as patients with GS are usually diagnosed in adulthood during routine investigation. Symptoms reported in the literature range from asymptomatic, to mild symptoms of cramps and fatigue, to severe manifestations such as tetany, paralysis, and rhabdomyolysis. This is the first systematic evaluation of a large group of patients with genetically defined GS. METHODS: We evaluated the symptoms and quality of life (QOL) in 50 adult GS patients with confirmed mutations in NCCT, using a standardized questionnaire. This cohort was compared with 25 age- and sex-matched controls. RESULTS: GS patients were significantly more symptomatic than controls. The most common symptoms were salt craving, with musculoskeletal symptoms such as cramps, muscle weakness, and aches and constitutional symptoms such as fatigue, generalized weakness and dizziness, and nocturia and polydipsia. Forty-five percent of GS patients consider their symptoms a moderate to big problem. Measures of health-related QOL were significantly lower in GS patients compared with controls, particularly in terms of role limitations caused by physical health, emotion, level of energy, and general health perception. CONCLUSIONS: This descriptive study indicates that GS is not an asymptomatic disease and adversely affects QOL in these patients. Further studies are needed to assess the impact of therapy on symptoms and QOL.

Midodrine: a selective alpha-adrenergic agonist for orthostatic hypotension and dialysis hypotension.

Midodrine is an oral agent which acts as a selective peripherally-acting alpha-receptor agonist. Midodrine is a prodrug that is almost completely absorbed after oral administration and converted into its active drug de-glymidodrine in the systematic circulation, with a bioavailability of 93%. It has been used successfully in the treatment of neurogenic orthostatic hypotension and more recently, in the treatment of dialysis hypotension. It acts through vasoconstriction of the arterioles and the venous capacitance vessels, thereby increasing peripheral vascular resistance and augmenting venous return, respectively. It is a unique agent in the armamentarium against orthostatic hypotension since it has minimal cardiac and CNS effects. This article will review the literature on midodrine for conditions of autonomic dysfunction, with focus on recent studies on its use in haemodialysis patients.

Midodrine and cool dialysate are effective therapies for symptomatic intradialytic hypotension.

Intradialytic hypotension (IDH) is a morbid complication of hemodialysis (HD). Both midodrine, an oral selective alpha1 agonist, and cool dialysate have been reported as useful therapies for this problem. We performed this prospective crossover study to compare the efficacy of these two therapies, alone and in combination, for IDH. The study consisted of a control phase and three treatment phases: midodrine phase (10 mg oral dose pre-HD), cool dialysate phase (35.5 degrees C), and combination therapy phase (midodrine, 10 mg, and dialysate temperature, 35.5 degrees C). Each phase consisted of nine consecutive HD treatments. Eleven patients (six men, five women; mean age, 67.5 years) with known symptomatic IDH were studied. This cohort was followed up in terms of blood pressure measurements (pre-HD blood pressure, lowest intradialytic blood pressure, post-HD blood pressure), weights, laboratory values, and interventions for IDH. The lowest intradialytic blood pressures were significantly better with midodrine and cool dialysate compared with the control phase (systolic blood pressure [SBP], 103.9 +/- 4.1 [mean +/- standard error of the mean] and 102.6 +/- 2.9 v 90.6 +/- 2.5 mm Hg, respectively; P < 0.001), as were the post-HD blood pressures (SBP, 116.9 +/- 4.0 and 118.2 +/- 3.5 v 109.0 +/- 2.1 mm Hg; P < 0.01). In addition, the lowest intradialytic blood pressures were significantly better with the combination phase compared with the control phase (SBP, 103.7 +/- 4.2 v 90.6 +/- 2.5 mm Hg; P < 0.001), as were the post-HD blood pressures (SBP, 122.1 +/- 4.6 v 109.0 +/- 2.1 mm Hg; P < 0.01). There was a significant reduction in the number of nursing interventions performed and volume of saline infused for IDH with midodrine and cool dialysate compared with control. There was a trend toward amelioration of hypotensive symptoms with both therapies. Laboratory values, including Kt/V, did not change significantly with either midodrine or cool dialysate. This prospective study shows that both midodrine and cool dialysate are effective therapies for symptomatic IDH. There does not seem to be additional benefit when these two therapies are used in combination.

Midodrine is effective and safe therapy for intradialytic hypotension over 8 months of follow-up.

Intradialytic hypotension (IDH) is a common and frustrating complication of hemodialysis. Certain end stage renal disease (ESRD) patients recurrently manifest this disabling condition. Both patient-specific factors (autonomic insufficiency, cardiac disease) and dialysis treatment-related factors (ultrafiltration, increased core body temperature) are thought to have significant causative roles. Most therapeutic interventions to date have been either unsuccessful or poorly tolerated. However, recent studies have shown that midodrine, an oral peripheral alpha-1 adrenergic agonist, is an effective and safe therapy for symptomatic IDH in the short-term. We report our experience with the predialysis use of midodrine for IDH in 13 hemodialysis (HD) patients over a 5 to 8 month period. Thirteen patients (8 male, 5 female, mean age 63.9 yrs) with recurrent symptomatic IDH were given midodrine 10 mg orally 30 min before each HD session. Blood pressures (pre-HD BP, lowest intradialytic [ID] BP, post-HD BP) and body weights were tracked for each HD treatment. Values for 10 HD sessions prior to midodrine therapy (Baseline) were compared to values (10 HD sessions each) during the 1st, 5th and 8th month of midodrine therapy. Data were analyzed using ANOVA for repeated measures and paired t-tests, with each patient serving as his/her own control. Patients were monitored for 5 months (n = 13) and 8 months (n = 8), respectively. All lowest intradialytic BPs, post-HD SBPs, and MAPs were significantly improved (p <0.05) on midodrine therapy. This effect was maintained during all periods of follow-up. There was no significant difference in mean albumin, hematocrit, Kt/V, calcium, and sodium between baseline and all periods of follow-up. Mean ultrafiltration volume per HD session was not significantly different than baseline over the course of study. A subjective improvement in hypotensive symptoms was also noted. Importantly, there were no adverse reactions to midodrine in all periods of follow-up. Midodrine appears to be an effective and safe treatment for HD patients with symptomatic IDH, and remains beneficial when used for an extended period of time.

Drug-induced acute tubulointerstitial nephritis: the clinical spectrum.

Clinical and laboratory findings vary with the drug involved. A definitive diagnosis requires renal biopsy; a gallium scan may be helpful when biopsy is not feasible. Outcome depends on drug withdrawal, but corticosteroids may be beneficial.

Intradialytic hypotension: is midodrine beneficial in symptomatic hemodialysis patients?

Symptomatic hypotension during hemodialysis is a disabling complication in end-stage renal disease (ESRD) patients, especially in certain groups of patients who are at higher risk for this problem. Autonomic dysfunction is thought to play a significant role. We evaluated the efficacy of midodrine, an oral agent with selective alpha-adrenergic agonist activity used in the treatment of neurogenic orthostatic hypotension, on 10 hemodialysis patients with persistent intradialytic hypotension. The patients were given a dose of midodrine (mean dose, 5.5 mg; range, 5 to 10 mg) 30 minutes before each hemodialysis session. We compared blood pressure, pulse, body weight, and laboratory values for 10 consecutive dialysis sessions off and on midodrine therapy. There was a statistically significant improvement in lowest intradialytic systolic blood pressure (from 96.6 to 114.7 mm Hg; P < 0.001), lowest intradialytic diastolic blood pressure (from 53.2 to 59.0 mm Hg; P = 0.002), lowest intradialytic mean arterial pressure (from 67.7 to 77.6 mm Hg; P < 0.001), posthemodialysis systolic blood pressure (from 116.5 to 127.1 mm Hg; P < 0.001), posthemodialysis diastolic blood pressure (from 66.6 to 69.7 mm Hg; P = 0.040), and posthemodialysis mean arterial pressure (from 83.2 to 88.8 mm Hg; P = 0.001) after patients were placed on midodrine. There also was a small but statistically significant decrease in intradialytic pulse rate (from 86.3 to 81 beats/min; P = 0.021) and posthemodialysis pulse rate (from 87.4 to 81.7 beats/min; P = 0.024) after initiation of midodrine therapy. There was no significant difference in any of the prehemodialysis blood pressure measurements or pulse rate off or on midodrine therapy. The improvements in intradialytic and posthemodialysis blood pressure were associated with a uniform subjective improvement in symptoms associated with dialysis hypotension, such as cramps, fatigue, dizziness, and weakness. Other than scalp paresthesia in one patient, no adverse effects were noted. Our results suggest that the administration of a single dose of midodrine before hemodialysis is an effective therapy for intradialytic hypotension. A prospective trial with adequate patient numbers and long-term follow-up would be useful to evaluate this drug's efficacy and safety profile in patients with ESRD.

Biochemical aberrations in a dialysis patient following parathyroidectomy.

Renal osteodystrophy is a common problem in patients with end-stage renal disease. Severe secondary hyperparathyroidism unresponsive to an intensive regimen of diet, phosphate binders, and calcitriol therapy is an indication for surgical parathyroidectomy. Certain unique postoperative electrolyte aberrations are seen after parathyroidectomy, including severe hypocalcemia and hypophosphatemia (hungry bone syndrome), as well as hyperkalemia. Identifying the patient at high risk for developing these electrolyte abnormalities will facilitate perioperative and postoperative management.