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Wilfred Druml

Publications and source records attributed to Wilfred Druml.

At least 19 recordsLinked to original sources
PubMed2006

A woman with red eyes and hypokalemia: a case of acquired Gitelman syndrome.

Gitelman syndrome is a rare hereditary disorder of the thiazide-sensitive NaCl transporter in the distal renal tubular cells, but mimicking of such hereditary tubular disorders has been described in different autoimmune diseases (Sjögren syndrome, SLE, ...). A 62-year-old woman with painful red eyes and sicca syndrome presented at the ophthalmological department. The diagnostic evaluation identified a Sjögren syndrome with early endophthalmitis as the reason for the red eyes. Results of laboratory examination indicated severe hypokalemia, metabolic alkalosis and hypomagnesemia, although this had not been seen years earlier. Together with the urine analysis, a rare case of an acquired Gitelman syndrome was diagnosed. Substitution with potassium and magnesium improved the initial symptoms of weakness, but renal electrolyte wasting persisted even after treatment of Sjögren syndrome. In patients with autoimmune disease, laboratory analysis of serum electrolytes should be performed because different acquired tubular disorders can lead to severe hypokalemia.

Bartter Syndrome↗
PubMed2005

Peritransplant immunoadsorption: a strategy enabling transplantation in highly sensitized crossmatch-positive cadaveric kidney allograft recipients.

BACKGROUND: Kidney transplant recipients with a current positive complement-dependent cytotoxicity crossmatch (CDCXM) are at high risk for hyperacute rejection and graft loss. Immunoadsorption (IA) represents an efficient strategy to remove donor-specific alloantibodies. In this analysis, we evaluated effectiveness of peritransplant IA as an anti-humoral strategy to overcome a current positive CDCXM in presensitized renal allograft recipients. METHODS: Between 1999 and 2003, 40 high risk cadaveric kidney allograft recipients (median CDC panel reactive antibody [PRA] level, 77%; number of retransplants, n = 38) were subjected to peritransplant IA with protein A (one pretransplant IA session followed by a course of repeat posttransplant IA sessions) in addition to preemptive antilymphocyte antibody therapy. RESULTS: In nine of these patients, a current positive CDCXM was rendered negative by a single pretransplant IA session. Thirty-one recipients had a negative CDCXM already before pretransplant IA. No difference in graft survival was found between CDCXM-positive and CDCXM-negative recipients (3-year graft survival, 78% vs. 71%, P = 0.6). Comparable rates of immunological graft loss at 3 years were observed (11% vs. 13%, P = 0.8). Patient groups did not significantly differ with respect to median serum creatinine at 1 year (1.23 mg/dL [CDCXM-positive] vs. 1.57 mg/dl [CDCXM-negative], P = 0.07) and at the end of follow-up (median 32 months; 1.19 mg/dL vs. 1.63 mg/dL, P = 0.06). Moreover, patient groups showed similar rates of biopsy-proven cellular rejection (11% vs. 20%) or C4d-positive graft dysfunction (33% vs. 32%). CONCLUSION: Our results demonstrate that peritransplant IA enables successful cadaveric kidney transplantation in the context of a positive CDCXM.

Adult↗
PubMed2005

Citrate kinetics in patients receiving long-term hemodialysis therapy.

BACKGROUND: Regional anticoagulation using sodium citrate is used increasingly in hemodialysis patients at high risk for bleeding. However, citrate metabolism has never been evaluated systematically in hemodialysis patients, and it remains to be shown that citrate is cleared adequately in the presence of renal dysfunction. This study compares the pharmacokinetics of citrate in hemodialysis patients with minimal residual function with that in patients with normal renal function. METHODS: Long-term hemodialysis patients (n = 7) and patients without renal failure (n = 11) were investigated during routine immunoadsorption treatment by using a standardized citrate infusion protocol. Serial analysis of blood samples was performed before, during, and up to 120 minutes after citrate infusion (0.33 mmol/kg/h). Citrate plasma concentrations were measured colorimetrically. In addition, ionized calcium, pH, and bicarbonate were measured by using a blood gas analyzer. RESULTS: Basal (0.09 +/- 0.03 versus 0.12 +/- 0.03 mmol/L; P = not significant) and peak citrate concentrations were similar in both groups (1.24 +/- 0.42 versus 1.19 +/- 0.33 mmol/L; P = not significant). Citrate clearance was similar in patients with renal failure (0.31 +/- 0.06 L/min) and controls (0.35 +/- 0.11 L/min; P = 0.47). Effects on pH were minimal and did not differ between groups. No patient developed complications from citrate infusion. CONCLUSION: Compared with controls, citrate clearance and metabolism in long-term hemodialysis patients is not impaired, and no significant acid-base disorder occurred during citrate anticoagulation. From these data, it is tempting to conclude that citrate anticoagulation can be used safely in patients with chronic renal failure on regular hemodialysis therapy.

Acid-Base Imbalance↗
PubMed2005

Nutritional management of acute renal failure.

Acute renal failure (ARF) is associated with fundamental alterations of metabolism and immunocompetence with the induction of a pro-oxidative and proinflammatory state. Thus, the objectives of nutritional therapy include not only conventional goals such as maintaining lean body mass and stimulating immunocompetence and repair functions, but also mitigating the inflammatory state and improving the oxygen radical scavenging system and endothelial functions. Moreover, pre-existing and/or hospital-acquired malnutrition has been identified as an important factor contributing to the persistent high mortality in acutely ill patients with ARF. A nutritional program for a patient with ARF must consider not only the specific metabolic consequences associated with renal failure and with the underlying disease process, but also the profound alterations in nutrient balances induced by replacement therapy. Nutrient requirements thus may differ widely between individual patients and during the course of disease, and nutrition therapy must be coordinated with renal replacement therapy. Whenever possible, enteral nutrition should be provided in patients with ARF because even small amounts of luminal nutrients will help to maintain intestinal function. Nevertheless, in many patients parenteral nutrition, at least supplementary and/or temporarily, will become necessary. Because of the complex alterations in the use of various nutrients and the impaired tolerance to electrolytes and volume load, metabolic complications of nutritional support frequently occur in patients with ARF. Therefore, nutrition therapy must be more closely monitored in patients with ARF than with other diseases.

Acute Kidney Injury↗
PubMed2004

Ascites and intraabdominal infection.

PURPOSE OF REVIEW: This review will give an overview of current trends in diagnosis, treatment, and pathogenesis of ascites and intraabdominal infection in cirrhotic and noncirrhotic critically ill patients. RECENT FINDINGS: Single clone-bacterial DNA has been found in sterile ascites and serum, proving the concept of direct translocation. Activation of mesenteric macrophages can be induced by splanchnic vasodilatation but also by hypoxia. Carbon monoxide, an end product of heme catabolism, promotes splanchnic vasodilatation, representing a possible link between gastrointestinal hemorrhage and circulatory dysfunction. Colorimetric test strips and automated counters accurately diagnose spontaneous bacterial peritonitis. Vasopressin V2-antagonists have been introduced as novel therapy for impaired water excretion in hyponatremia. SUMMARY: Emerging pathophysiological concepts have modified the conventional view of hydrostatic and Starling forces in the evolution of ascites. Current data indicate that the dynamic sequence of bacterial translocation, mesenteric inflammation, splanchnic vasodilatation and intrahepatic vasoconstriction determines occurrence, severity, and outcome of ascites and intraabdominal infection.

Ascites↗
PubMed2004

Minimal changes of serum creatinine predict prognosis in patients after cardiothoracic surgery: a prospective cohort study.

Acute renal failure increases risk of death after cardiac surgery. However, it is not known whether more subtle changes in renal function might have an impact on outcome. Thus, the association between small serum creatinine changes after surgery and mortality, independent of other established perioperative risk indicators, was analyzed. In a prospective cohort study in 4118 patients who underwent cardiac and thoracic aortic surgery, the effect of changes in serum creatinine within 48 h postoperatively on 30-d mortality was analyzed. Cox regression was used to correct for various established demographic preoperative risk indicators, intraoperative parameters, and postoperative complications. In the 2441 patients in whom serum creatinine decreased, early mortality was 2.6% in contrast to 8.9% in patients with increased postoperative serum creatinine values. Patients with large decreases (DeltaCrea <-0.3 mg/dl) showed a progressively increasing 30-d mortality (16 of 199 [8%]). Mortality was lowest (47 of 2195 [2.1%]) in patients in whom serum creatinine decreased to a maximum of -0.3 mg/dl; mortality increased to 6% in patients in whom serum creatinine remained unchanged or increased up to 0.5 mg/dl. Mortality (65 of 200 [32.5%]) was highest in patients in whom creatinine increased > or =0.5 mg/dl. For all groups, increases in mortality remained significant in multivariate analyses, including postoperative renal replacement therapy. After cardiac and thoracic aortic surgery, 30-d mortality was lowest in patients with a slight postoperative decrease in serum creatinine. Any even minimal increase or profound decrease of serum creatinine was associated with a substantial decrease in survival.

Adolescent↗
PubMed2003

Cholesterol improves the utilization of parenteral lipid emulsions.

Lipid emulsions have become an indispensable component of parenteral nutrition. Commercially available emulsions mostly have an identical composition of triglycerides (from plant oils) and egg-yolk phospholipids as emulsifier. Previous attempts to improve the composition of lipid emulsions have focused mainly on the triglyceride moiety. In the first fundamental modification of a lipid emulsion since their broader introduction into clinical medicine, we included free cholesterol in a lipid emulsion. We evaluated elimination and hydrolysis of triglycerides and lipid oxidation (by indirect calorimetry) in 10 healthy male normolipemic volunteers, comparing a conventional lipid emulsion (20% triglycerides) with an otherwise identical emulsion with the addition of 4 g/l free cholesterol. The rise in plasma triglycerides was mitigated during infusion of the cholesterol-enriched solution (323.8 +/- 27.5 vs. 202.0 +/- 18.9 mg.dL-1, p < 0.001), plasma half-life was reduced (41.6 +/- 5.4 vs. 29.3 +/- 5.1 min, p < 0.05), and total-body clearance was enhanced (0.96 +/- 0.1 vs. 1.52 +/- 0.2 ml.b.w.(.)min-1, p < 0.02). The rise in plasma free fatty acids (400.7 +/- 39.0 vs. 532.2 +/- 64.0 mumol.L-1; p < 0.02) and ketone bodies (beta-hydroxybutyrate) (151.6 +/- 37.0 vs. 226.3 +/- 33.01 mumol.L-1; p < 0.02) was augmented. Increases in plasma insulin and glucagon were less pronounced (p < 0.05). The fall in respiratory quotient was greater and the fraction of lipid oxidation as a percentage of total energy expenditure was increased (66.2% +/- 6.0 vs. 70.9% +/- 6.3, p < 0.05) during infusion of the modified solution. No impairment of gas exchange or other side effects were observed. Taken together these results indicate that the elimination of a cholesterol-supplemented lipid emulsion is accelerated, triglyceride hydrolysis is enhanced, and lipid oxidation is augmented. Thus, addition of cholesterol to a lipid emulsion might not only present a means of providing cholesterol in parenteral nutrition but also help to reshape artificial lipid particles to a more chylomicron-resembling composition and improve lipid utilization.

Adult↗
PubMed2003

Gastrointestinal disorders of the critically ill. Systemic consequences of ileus.

Ileus refers to the partial or complete blockage of the small and/or large intestine either by functional (adynamic or paralytic ileus) or mechanical bowel obstruction. The diffuse gastrointestinal dysmotility during functional and mechanical ileus may result in intestinal dilatation, increased luminal pressure and gut wall ischaemia which may lead to increased intra-abdominal pressure (IAP). Any type of ileus may promote abdominal fluid sequestration with severe systemic hypovolaemia, intestinal bacterial overgrowth with the evolution of bacterial translocation and systemic invasive infections and inflammation of the intestinal wall with concomitant release of cytokines and the development of the systemic inflammatory response syndrome. The most serious complications of ileus are mediated by an increase in IAP. Intra-abdominal hypertension has been found in up to 20% of critically ill patients and may lead to a broad pattern of systemic consequences with multiple organ dysfunction, including cardiovascular, hepatic, pulmonary, renal and neurological function. The abdominal compartment syndrome is an emergency condition which is defined as elevation of IAP above 20 to 25 mmHg and the presence of systemic consequences. Therapeutic considerations include the maintenance of adequate hydration status, avoidance of drugs known to impair intestinal perfusion, stimulation of gastric and intestinal motility and various nutritional aspects. Colonic tube placement after decompressive colonoscopy may be effective in reducing intestinal dilatation. In the abdominal compartment syndrome the 'open abdominal approach' with decompressive laparotomy by opening the peritoneal cavity and temporary abdominal closure is the therapy of choice.

Critical Illness↗
PubMed2002

The beginning of organ transplantation: Emerich Ullmann (1861-1937).

Between 1880 and 1930 there was a rapid surge in experiments with tissue transplantation, initially mainly of endocrine tissues (thyroid, parathyroid, testicles, ovary, adrenals etc.) with the aim of replacing endocrine function. Emerich Ullmann (1861-1937), who was born in Pecs, Hungary and worked his whole life as a surgeon in Vienna was the first to perform transplantations of solid organs in the modern sense of medicine. During 1899 and 1900 he conducted several experiments with intestinal transplantation and must be regarded as the father of intestinal transplantation--a hitherto unknown fact. He then moved to kidney transplantation and on March 7, 1902 he demonstrated a dog with a functioning kidney graft anastomized to the collar vessels with urine dripping off the ureter sutured to the skin of the neck in the lecture hall of the Society of Physicians in Vienna. Ullmann was the first to perform kidney auto-, homo- and heterotransplantations and in 1902 also tried--unsuccessfully--to perform the first human kidney transplantation using a pig kidney which he anastomized into the cubital region of a women with end stage renal disease. Ullmann also performed tissue transplantations (skin, testicles, ovaries) and made other scientific discoveries and described several novel surgical techniques. Finally, in 1914 he wrote the first monograph on the state of the art of transplantation medicine, a booklet on "Tissue and Organ Transplantation" summarizing the surprisingly extensive experience in transplantation medicine of his time. With the obvious immunologic barriers to transplantation, the first "technical surgical period" of transplantation came to an end around the times of Ullmann's death and clinical transplantation was not to be revived before effective means of immunosuppression became available in the 1950s.

Animals↗