Gastrointestinal Fluid Loss Research Articles

Acute kidney injury and electrolyte disorders in COVID-19.

Acute kidney injury (AKI) and electrolyte disorders are important complications of hospitalized coronavirus disease 2019 (COVID-19) patients. AKI is thought to occur due to multiple pathophysiological mechanisms, such as multiple organ dysfunction (mainly cardiac and respiratory), direct viral entry in the renal tubules, and cytokine release syndrome. AKI is present in approximately one in every ten hospitalized COVID-19 patients. The incidence rates of AKI increase in patients who are admitted to the intensive care unit (ICU), with levels higher than 50%. Additionally, renal replacement therapy (RRT) is used in 7% of all AKI cases, but in nearly 20% of patients admitted to an ICU. COVID-19 patients with AKI are considered moderate-to-severe cases and are managed with multiple interdisciplinary conducts. AKI acts as a risk factor for mortality in severe acute respiratory syndrome coronavirus 2 infection, especially when RRT is needed. Electrolyte disorders are also common manifestations in hospitalized COVID-19 patients, mainly hyponatremia, hypokalemia, and hypocalcemia. Hyponatremia occurs due to a combination of syndrome of inappropriate secretion of antidiuretic hormone and gastrointestinal fluid loss from vomiting and diarrhea. When it comes to hypokalemia, its mechanism is not fully understood but may derive from hyperaldosteronism due to renin angiotensin aldosterone system overstimulation and gastrointestinal fluid loss as well. The clinical features of hypokalemia in COVID-19 are similar to those in other conditions. Hypocalcemia is the most common electrolyte disorder in COVID-19 and seems to occur because of vitamin D deficiency and parathyroid imbalance. It is also highly associated with longer hospital and ICU stay.

Unaccounted for enteral volume loss linked to delayed cerebral ischemia after subarachnoid hemorrhage

Delayed ischemic neurological deficit (DIND) is seen as a clinical manifestation of cerebral vasospasm and is a significant cause of morbidity and mortality following aneurysmal subarachnoid hemorrhage (aSAH). Currently, the standard of care for DIND prevention in patients who have sustained aSAH is prophylactic nimodipine therapy and ensuring adequate fluid intake, alongside other treatments such as bowel care. Osmotic laxatives trap water within the bowel lumen to accelerate the transport of the gut contents through the bowel. Given the potential for DIND secondary to cerebral vasospasm, it is perhaps counterintuitive that gastrointestinal fluid loss and use of osmotic laxatives are not commonly considered in many aSAH management protocols. A retrospective case note analysis was performed for all adult patients (aged > 16 years) admitted to the Department of Neurosurgery at Leeds General Infirmary with a diagnosis of aSAH between August 2019 and September 2020. A total of 105 patients were included, 62% of whom were female, with a mean and median age of 54 years (range 24-84 years). Diarrhea was noted in 12 patients (11.4%), 58% of whom subsequently developed DIND (OR 15.30, CI 3.92-59.14; p = 0.0001). All patients received osmotic laxatives (97% having received ≥ 2 laxative agents). Patients with aSAH who subsequently developed diarrhea had significantly increased odds of developing DIND. Enteral volume loss due to osmotic laxative use is a potential risk factor for DIND after aSAH.

Case Report: Newborns With Pseudohypoaldosteronism Secondary to Excessive Gastrointestinal Losses Through High Output Stoma

Life-threatening electrolyte imbalance is not uncommon in preemies. Differential diagnosis is important for immediate treatment. The syndrome of pseudohypoaldosteronism (PHA) is characterized by increased aldosterone secretion associated with clinical signs of hypoaldosteronism reflecting mineralocorticoid resistance. There are type I, type II, and secondary type of PHA. Most secondary PHA reported in the pediatric population result from urinary infection and obstructive uropathy and extremely rarely from gastrointestinal fluid loss. Seven preemies accepted jejunostomy or ileostomy, and they suffered from high output stoma. Electrolyte imbalance with bodyweight loss or cardiac event was noted. We found a high level of aldosterone and renin and diagnosed them with secondary PHA due to excessive gastrointestinal losses. After stomal reversal, aldosterone and renin level became normalized, and electrolyte was corrected. This study reports the finding of secondary pseudohyperaldosteronism (hyponatremia, hyperkalemia, and metabolic acidosis) in a series of cases with intestinal resection and ostomy of different causes. Early stomal reversal was recommended.

Do the etiology of hyponatremia and serum sodium levels affect the length of hospital stay in geriatric patients with hyponatremia?

BackgroundHyponatremia can lead to a prolonged hospital stay and increased morbidity and mortality rates in geriatric patients. This study aimed to evaluate the effects of hyponatremia etiology and serum sodium (Na) levels on hospitalisation time in geriatric patients hospitalised due to hyponatremia.MethodsThe demographic characteristics, laboratory data, etiology of hyponatremia, and length of hospital stay were retrospectively recorded for 132 patients over 65 years of age who were hospitalised for hyponatremia.ResultsOf the 132 patients, 90 were female (68.2%), and 42 were male (31.8%). The serum Na levels of 66 (50%) patients were <120 mmol/L, those of 64 (48.5%) patients were 120-129 mmol/L, and those of two (1.5%) patients were >130 mmol/L. One hundred nine (82.6%) patients had hypoosmolar hyponatremia, 14 (10.6%) patients had isoosmolar hyponatremia, and nine (6.8%) patients had hyperosmolar hyponatremia. Also, 19.7% of the patients were hypovolemic, 37.9% were euvolemic, and 42.4% were hypervolemic. Hyponatremia etiology was congestive heart failure in 38 (28.8%) patients, syndrome of inappropriate antidiuretic hormone in 29 (22.0%) patients, gastrointestinal fluid loss in 24 (18.2%) patients, renal pathologies in 20 (15.2%) patients, the presence of drugs in 20 (15.2%) patients, and hypocortisolemia in one (0.8%) patient. The mean length of hospital stay for the patients was five (1-60) days. There was no statistically significant difference between the lengths of hospital stay based on hyponatremia etiology and serum Na levels (p=0.861 and p=0.076). It was observed that the lengths of stay for patients who developed hyponatremia during their hospitalisation in various clinics were longer than those for patients who presented to the emergency department (p<0.001).ConclusionsIn this study, it was determined that the length of hospital stay did not change with the etiology of hyponatremia and serum Na level at the time of admission, but patients who developed hyponatremia during their hospitalisation had longer hospitalisation times.

The association between gastrointestinal fluid losses and delayed ischaemic neurological deficit in aneurysmal subarachnoid haemorrhage

The association between gastrointestinal fluid losses and delayed ischaemic neurological deficit in aneurysmal subarachnoid haemorrhage

Use of standard formulations in pediatric home parenteral nutrition – the experience of a portuguese center during the COVID-19 pandemic

Rationale: Standard solutions for parenteral nutrition (PN) are safe and can meet the nutritional requirements of a significant number of pediatric patients. However, they may not always meet the individual requirements of those on long term PN, particularly those with significant gastrointestinal fluid losses. We evaluated the possibility of replacing individually tailored prescription for standard formulations in children on home PN.

Intractable Normal Anion Gap Metabolic Acidosis in a Patient with Diabetic Ketoacidosis

High anion gap metabolic acidosis (HAGMA) is a hallmark of Diabetic Ketoacidosis (DKA). Occasionally, a Normal Anion Gap Metabolic Acidosis (NAGMA) can be seen, especially during the treatment phase. In this case report, a 55-year-old lady with diabetes mellitus who presented with a 2-day history of fever, lethargy and multiple episodes of vomiting and diarrhoea. Initial laboratory investigations revealed: capillary blood glucose as 27 mmol/L, urine ketone as 3+, blood ketone as 3.5 mmol/L, serum bicarbonate as 14 mmol/L, and serum chloride as 95 mmol/L. She was treated with intravenous normal saline fluid resuscitation and constant rate insulin infusion which was fortunately accompanied by stabilization of blood glucose and normalization of blood ketone to 0.2 mmol/L. However, despite normalization of her anion gap (25 to 14), she remained unwell with acidotic breathing due to refractory hyperchloraemic NAGMA with bicarbonate at 11 mol/L and chloride of 112 mmol/L. It was then decided to administer 100 mL of 8.4% Sodium Bicarbonate solution. The next day, she was no longer tachypneic as her bicarbonate and carbon dioxide improved to 21 mmol/L and 32 mmHg respectively. The presence of NAGMA in DKA should prompt clinicians to conduct a thorough search for possible underlying causes, such as gastrointestinal fluid loss, sepsis and chloride load from aggressive fluid resuscitation with normal saline. Sodium bicarbonate should only be considered in intractable cases to correct a NAGMA and not routinely used in the treatment of DKA.

Hypovolemic Hyponatremia.

The etiology of hyponatremia is often multifactorial. The most common causes include hypovolemia from gastrointestinal (GI) or other fluid losses, thiazide diuretics, and SIAD [<citeref rid="ref1">1</citeref>]. In this chapter, we will discuss hypovolemic hyponatremia, as well as the clinical parameters that help distinguish between hypovolemic and euvolemic states. These include not only the urine [Na+] concentration but also the fractional uric acid excretion, a parameter that can be employed even when diuretics have been prescribed [<citeref rid="ref2">2</citeref>,<citeref rid="ref3">3</citeref>,<citeref rid="ref4">4</citeref>,<citeref rid="ref5">5</citeref>,<citeref rid="ref6">6</citeref>,<citeref rid="ref7">7</citeref>]. Among the common causes of hypovolemic hyponatremia are GI fluid loss, a range of endocrinopathies [<citeref rid="ref7">7</citeref>], and thiazide-induced hyponatremia, which is best considered as a distinct entity, in particular because recent data suggest that it has a genetic predisposition. Also, the discontinuation of thiazide is a key step in treatment [<citeref rid="ref2">2</citeref>,<citeref rid="ref7">7</citeref>]. The management of hypovolemic hyponatremia starts with confirming its presence and determining the underlying cause. Correction focuses on the appropriate use of isotonic fluid to effect volume repletion while avoiding an overly rapid rise in serum [Na+] concentration.

Frequency and Types of Hyponatremia in Stroke Patients Admitted in a Referral Neuroscience Institute of Dhaka

Background: Hyponatremia is a common electrolyte abnormality in acute stroke patients and may be related to variable etiology. Objective: To observe the frequency and types of hyponatremia in hospitalized acute stroke patients. Materials and methods: This cross-sectional study, carried out in a referral neuroscience institute of Dhaka during February to November 2017, included 209 patients admitted with acute stroke (65 ischemic, age 61.5±13.3 years, M/F: 45/20; 144 hemorrhagic, age 59.2±13.1 years, M/F: 80/64). The clinical and laboratory values on admission were recorded. Those having hyponatremia (serum sodium <135 mmol/L) on admission were evaluated by clinical features (history of vomiting or diarrhoea, volume status, urine output) and laboratory parameters (urine osmolality, urine sodium, plasma osmolality, blood urea, hematocrit) to determine the types of hyponatremia. Results: Four patients died before the serum could be sent for electrolytes. Among the rest, 36 (17.6%) had hyponatremia on admission. Serum sodium level was <125 mmol/L in 7 (19.4%) and 125-134 mmol/L in rest of the patients having hyponatremia (29; 80.6%). The frequency of hyponatremia was similar in ischemic and hemorrhagic stroke (17.2% vs. 17.7%, p=0.925). Syndrome of inappropriate antidiuresis (SIAD) was most frequent cause of hyponatremia (50.0%), followed by cerebral salt wasting (CSW; 30.6%). The rest had either hyponatremia related to gastrointestinal (GI) fluid loss (2.8%) or died before a cause of hyponatremia could be ascertained (11.1%). There was no significant difference of age, gender, NIHSS score and GCS score on admission as well as in hospital stay and in-hospital mortality between patients with or without hyponatremia (p=ns for all). Frequency of CSW was relatively higher in hemorrhagic stroke (hemorrhagic vs. ischemic: 32.0% vs. 27.3%) and SIAD in ischemic stroke (hemorrhagic vs. ischemic: 40.0% vs. 72.7%) but did not reach level of statistical significance. Conclusion: Frequency of hyponatremia seems remarkable in hospitalized acute stroke patients, SIAD and CSW being the most frequent cause.

Loperamide therapy for voluminous diarrhea in Ebola virus disease.

Loperamide therapy for voluminous diarrhea in Ebola virus disease.

Hyponatriämie

Hyponatremia is the most common electrolyte disorder in the hospital setting and is defined as a serum sodium concentration less than 135mmol/l. Most patients have mild hyponatremia (plasma sodium concentration 130-134mmol/l) and few if any symptoms. Serum sodium concentrations between 120 and 129mmol/l can be associated with lack of concentration, nausea, forgetfulness, apathy and loss of balance. Severe hyponatremia (<120mmol/l) can cause coma or grand mal seizure. If hyponatremia occurs acutely (duration <48h) it will cause more severe symptoms than are observed in chronic hyponatremia (>48h). It is important to distinguish between different types of hyponatremia: euvolemic hyponatremia causing syndrome of inappropriate antidiuretic hormone secretion(SIADH) also known as Schwartz-Bartter syndrome, hypervolemic hyponatremia (cardiac failure and liver cirrhosis) and hypovolemic hyponatremia (diarrhoea, vomiting or other gastrointestinal fluid losses). Increased levels of ADH and continued fluid intake are the pathogenetic causes of all three types of hyponatremia; nonetheless, infusion of isotonic fluid is the therapy of choice for hypovolemic hyponatremia. In contrast, fluid restriction, lithium carbonate, urea, loop diuretics or demeclocycline have been used as therapeutic options to correct hyponatremia in euvolemic or hypervolemic hyponatremia but most of these therapies have proven to be cumbersome and inefficient. Recently a new class of pharmacological agents has become available, the vaptans, orally taken vasopressin antagonists. Clinical trials showed them to provide effective, specific and safe therapy of hyponatremia. In Europe tolvaptan, the only such agent on the market is now approved for the treatment of euvolemic hyponatremia.

Prolonged Diarrheal Illness and Acute Liver Failure after Ingestion of Amatoxin Producing Gallerina Mushrooms

Purpose: Case Description: AS is a 44 yr old woman who picked wild mushrooms from her yard and cooked them into a soup. Eight hours following ingestion, she developed nausea and multiple episodes of non-bloody, nonbilious vomiting. Subsequently she developed diffuse abdominal pain and a foul smelling, watery diarrhea. Due to associated weakness, fevers and chills, she presented to the ED 14 hours after ingestion. In the ED the patient was found to have orthostatic hypotension due to gastrointestinal fluid loss. Initial liver tests, drawn 20 hours after ingestion, were within normal limits. Urinalysis was suggestive of UTI. The patient received IV fluids for presumed viral gastroenteritis and antibiotics for suspected UTI and admitted to the medical service for further management. Laboratory tests drawn 43 hours after ingestion showed that total bilirubin, AST, ALT, INR increased to 1.3 mg/dl, 360 U/L, 349 U/L, 1.5 respectively. At that point, a diagnosis of acute liver failure was made and the patient was started on N-acetylcysteine IV; penicillin G, 3 MU IV Q4hr; cimetidine 400 mg Q8hr; fentanyl for pain and aggressive fluid and electrolyte repletion. Over the next 36 hours AST peaked at 10,556, ALT peaked to 9,302, and INR peaked at 2.4. Liver chemistries improved over the next few days. The patient continued to have large volume bloody diarrhea which required aggressive fluid resuscitation and blood transfusion. C. difficile panel and stool culture were negative. No significant findings were detected on flexible sigmoidoscopy performed 10 days after presentation. Milk thistle was initiated due to reports of the active ingredient silybin as a treatment of amatoxin exposure. After 14 days, liver tests returned to baseline and the diarrhea slowed but did not fully resolve until weeks after initial presentation. Mushroom samples was obtained from patient's yard and sent to a mycology laboratory. Meixner test was positive for amatoxin and the mushroom was identified as Gallerina species. Conclusion: α-amanitin produced by Gallerina species can result in a prolonged diarrheal illness with bleeding in addition to acute liver failure due to significant enterohepatic circulation of the amatoxin and associated mucosal injury to the small bowel.

Prerenal azotemia from excessive sweating in an adult with a cystic fibrosis gene mutation

We present the case of a 58-year-old male with chronic kidney disease who was admitted to the hospital multiple times with extracellular fluid volume depletion and prerenal azotemia. Some episodes were associated with gastrointestinal fluid losses and others with profuse diaphoresis in the absence of gastrointestinal fluid losses. At the age of 57 years, a common cystic fibrosis transmembrane conductance regulator protein mutation and a family history of cystic fibrosis were documented. We hypothesize that the abnormal cystic fibrosis transmembrane conductance regulator resulted in repeated bouts of excessive sweating, extracellular fluid volume depletion, and acute renal failure. This case is unique because of the prolonged period of time over which multiple documented episodes of prerenal acute renal failure occurred and because of the onset of the episodes in adulthood.

Enfrentamiento de la hiponatremia: Más allá de la corrección del sodio. A propósito de un caso clínico

Hyponatremia can be a marker of an underlying disease. We report a 52 years-old male with Diabetes Mellitus who consulted for an episode of nausea and vomiting lasting four days. His baseline serum sodium was 118 mEq/L. He had no neurological deficit. Hyponatremia was initially interpreted in context of gastrointestinal fluid loss but correction with saline solution was poor. His urine sodium was 105 mEq/L and his urine osmolality was 281 mOsm/L, so an Inappropriate Secretion of Antidiuretic Hormone Syndrome was suspected. Later, we found that the patient had a two year history of fatigue, weakness, anorexia, frequent nausea, vomiting and diarrhea, loss of libido and decreased axillary and pubic hair. Thyroid-Stimulating Hormone (TSH) was normal and serum Cortisol < 1 µg/dL. A CT scan showed a sellar mass compatible with a macroadenoma. There was also a moderately high serum prolactin and low testosterone, thyroxin and growth hormone levels. The visual fi eld exami-nation showed right temporal hemianopsia. The patient was treated with steroids with a very good clinical response and serum sodium normalization. Subsequently a transsphenoidal excision of the tumor was performed and replacement of the other hormones was started. Now the patient remains asymptomatic.

Rotavirus: The challenges ahead

Diarrhea remains one of the most common illnesses of children worldwide.(1) Rotaviruses are the single most important etiologic agents of severe diarrhea among young children, responsible for 114 million cases, 25 - 55% of all hospital admissions for diarrhea and more than 610,000 deaths worldwide every year.(2) Rotavirus is ubiquitous and by the age of three to five years, 95% of the children worldwide would have been infected.(3) It is estimated that 82% of these deaths occur in developing countries (the third most common cause of death, with about two million deaths per year) equivalent to approximately 1,205 child deaths each day, because of poorer access to treatment and a greater prevalence of malnutrition.(2) In India, 350,000 children, under five, die every year due to diarrheal diseases, out of which one-third is due to rotavirus gastroenteritis. The prevalence of rotavirus diarrhea in India has been found to vary between 5 and 71% in hospitalized children < 5 years of age, with acute gastroenteritis.(4) Apart from the primary burden of rotavirus disease on childrens' health (mortality and morbidity), rotavirus also has a significant economic impact, which can be both direct and indirect. Examples of direct costs include medical costs resulting from hospitalizations, out patient visits, personnel, facilities, diagnostics, and medication. Indirect costs include those incurred to society and households as a result of lost work time when parents are forced to stay home to take care of sick children – resulting in reduction of labor productivity and loss of wages. Intangible costs such as pain and suffering add to the burden. A review of available preventive measures against rotavirus infection in relevance to India was hence undertaken. Rotavirus The rotavirus genus belongs to Reoviridae family of viruses. Rotaviruses are highly contagious and the predominant mode of transmission is the fecal–oral route.(3) It remains stable and infective in human feces for up to one week and can survive for weeks in recreational or drinking water, hence nosocomial infections are also widespread. Person-to-person spread, via contaminated hands, is probably the most important means by which rotaviruses are disseminated in close communities, such as hospitals and homes. Transmission among non-toilet trained children in nurseries and day care centers is facilitated by direct close contact, as well as sharing contaminated food, drinks or toys.(5) Asymptomatic excretion of rotavirus occurs in half of the infected children before the onset of clinical symptoms, and persists in one-third of the children a week after the symptoms end. Rotavirus infection is preceded by an incubation period of 24 – 48 hours. Symptoms range from vomiting and mild watery diarrhea of short duration to severe gastroenteritis with life-threatening dehydration, secondary to gastrointestinal fluid loss, a problem associated with developing countries. Significant rotavirus shedding occurs during an episode of diarrhea, but many infected individuals shed the virus without experiencing diarrhea. Respiratory transmission has been speculated because of (i) the high rates of infection in the first three years of life regardless of sanitary conditions, and (ii) the failure to document fecal oral transmission in several outbreaks of rotavirus over large geographic areas in the winter.(3,6) Published epidemiological studies covering 18 Indian cities (1996 – 2001) showed that G1 was the single most common serotype, and the burden of severe disease and hospitalization is borne predominantly by G1, G2, G3, G4, and G9.(7)

Treatment of Hyponatremia

Hyponatremia is an electrolyte disorder that is defined by a serum sodium concentration of less than 136 mmol/L. Hyponatremia occurs at a high incidence. It is commonly associated with mild to moderate mental impairment. Hypoosmolar hyponatremia occurs in the setting of plasma volume deficiency ("hypovolemia", e. g. after gastrointestinal fluid loss), liver cirrhosis and cardiac failure ("hypervolemic" hyponatremia) and syndrome of inappropriate antidiuretic hormone secretion ("euvolemic" hyponatremia). Excessive antidiuretic hormone and continued fluid intake are the pathogenetic causes of these hyponatremias. Whereas hypovolemic hyponatremia is best corrected by isotonic saline, conventional proposals for euvolemic and hypervolemic hyponatremia consist of the following: fluid restriction, lithium carbonate, demeclocycline, urea and loop diuretic. None of these nonspecific treatments is entirely satisfactory. Recently a new class of pharmacological agents -orally available vasopressin antagonists, collectively called vaptans- have been described. A number of clinical trials using vaptans have been performed already. They showed vaptans to be effective, specific and safe in the treatment of euvolemic and hypervolemic hyponatremia.

Diagnosis and treatment of acute renal failure in patients with cirrhosis

In patients with cirrhosis, acute renal failure is due to prerenal failure (a result of decreased renal perfusion) and tubular necrosis. There are 3 main causes of prerenal failure: 'true hypovolemia' (which complicates hemorrhage, gastrointestinal or renal fluid losses), sepsis, and type 1 hepatorenal syndrome (HRS). Prerenal failure may also be due to the administration of non-steroidal antiinflammatory drugs, or intravascular radiocontrast agents. Prerenal failure is reversible after restoration of renal blood flow. Treatments target the cause of hypoperfusion, and fluid replacement is used to treat 'non-HRS' prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy with terlipressin (combined with intravenous human albumin), noradrenaline (combined with albumin and furosemide) or midodrine (combined with octreotide and albumin) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for Molecular Adsorbent Recirculating System) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. Studies are needed on the natural course and treatment (e.g., renal-replacement therapy) of acute tubular necrosis in patients with cirrhosis.

Relationship between hydration estimate and body weight change after fluid therapy in critically ill dogs and cats

AbstractObjective: To characterize the relationship between clinical estimates of hydration in dogs and cats admitted to an intensive care unit (ICU) and changes in their body weight following 24–48 hours of fluid therapy.Design: Outcome study.Setting: ICU at a veterinary teaching hospital (VTH).Animals: A total of 151 dogs and 42 cats with various medical disorders that had not had surgery within 48 hours of admission into the ICU were consecutively admitted into the study. Animals with any condition predisposing to excess fluid loss or retention were excluded: heart disease, sepsis, trauma, pancreatitis, pleural or pericardial effusion, ascites, and pathologic oliguria. Animals that acquired any of the following during the observation period were excluded: gastrointestinal fluid loss, edema or diseases predisposing to edema, oliguria, diuretic therapy, and body fluid drainage or hemorrhage. Fluid therapy was ordered based on estimate of hydration at admission. Other treatments were not modified or withheld.Interventions: Physiologic data were collected at the time of admission and 24–48 hours later.Measurements and main results: Hydration was estimated on admission to the ICU using clinical judgement with no supporting laboratory data. Each admitting clinician used this estimate to plan fluid therapy. Fluid therapy was defined as the administration of any enteral or parenteral fluids as well as any decision to withhold fluids. Paired measurements taken on admission and at 24–48 hours included packed cell volume (PCV), total plasma solids (TS), and body weight. Amount and type of fluids or blood products administered were noted. Neither clinician estimates of dehydration nor baseline PCV or TS predicted clinically significant changes in body weight following fluid therapy, and there was no relationship between weight change and changes in PCV or TS.Conclusions: A clinical diagnosis of dehydration in our ICU does not predict weight gain following fluid therapy. Neither baseline PCV/TS nor changes in these measurements following 24–48 hours of fluid therapy predicted changes in body weight.

Spectrum of renal diseases in the elderly: single center experience from a developing country.

From November 1998 to March 2000, two hundred patients over the age of 60 years (Elderly) with clinical renal disease were studied. 144 patients were between ages of 60-69 years, 46 between 70-79 years and 10 were above 80 years. The elderly patients (Male 165; Female 35) with renal disease constituted 11% (200/1816) of the total nephrology consultation during the study period. The clinical presentation included chronic renal failure (42.5%); acute renal failure (28%); nephrotic syndrome (14.5%); acute glomerulonephritis (7.5%); renal vascular disease (5%) and renal cystic disease (2.5%). Diabetic nephropathy, obstructive uropathy and hypertensive nephrosclerosis were the major causes of CRF, accounting for 80% of total CRF in the elderly. Chronic glomerulonephritis and chronic pyelonephritis (CPN) were less common and etiology of CRF was uncertain in 5.9% of cases. However, diabetic nephropathy was the commonest (49.4%) cause of chronic renal failure. We did not see a single case of ischemic nephropathy causing CRF in the present study. Prerenal ARF, obstructive uropathy and sepsis were contributing factors for ARF in 82% of the cases. Volume depletion due to gastrointestinal fluid loss and urinary tract obstruction on account of enlarged prostate were the leading causes of ARF in 20 (35.7%) and 8 (14.3%) cases respectively. Sepsis with or without multiorgan failure was the major (46.7%) cause of mortality in patients with ARF and overall mortality was 26.8%. The commonest (31%) cause of nephrotic syndrome was the idiopathic membranous nephropathy. Diabetic nephropathy related to type-2 diabetes mellitus was the second most common (24.1%) cause of nephrotic syndrome. Diffuse endocapillary proliferative GN of post infectious etiology was the commonest (73.3%) type of acute GN in our elderly patients. Renal cystic diseases were noted in 5 (ADPKD 3; Simple cyst-2) patients. Thus, overall spectrum of renal disease in our elderly patients is similar to that of developed nations except in two ways: (i) Endocapillary proliferative GN of post infectious origin was the commonest type of acute GN and (ii) Rarity or absence of ischemic nephropathy and atherosclerotic renal artery occlusive disease.

Long-term follow-up of acute renal failure caused by angiotensin converting enzyme inhibitors

Angiotensin converting enzyme (ACE) inhibitors are useful in the treatment of hypertension and heart failure. However, acute renal failure (ARF) may occur in patients who are taking these drugs in situations associated with decreased glomerular filtration pressure, such as dehydration caused by acute diarrhea or diuretic therapy. Sixty-four patients who were admitted to the intensive care unit for ARF associated with ACE inhibitor therapy were followed for more than 5 years. In this historical retrospective study, we documented that 45 patients were treated for hypertension (group I) and 19 were treated for heart failure (group II). Their mean age was 71.2 ± 11.6 years. Patients with ARF presented with overt dehydration in 91% and 84% of the cases in groups I and II, respectively. Hypovolemia was caused by diuretics or gastrointestinal fluid loss. Bilateral artery-renal stenosis or stenosis in a solitary kidney was documented in 22% and 10% of patients in groups I and II, respectively. The probability of survival was 91% and 49% at 1 year and 64% and 18% at 5 years, for groups I and II, respectively. Acute renal failure required hemodialysis in seven patients, but none of them became dialysis dependent. In the subgroup of patients with preexisting chronic renal failure, all the patients except for one who belonged to group II died within 2 years. In both groups, after resolution of ARF, plasma creatinine concentration returned to baseline level and the course of renal function was not significantly worsened. In conclusion, ARF associated with ACE inhibitors is likely to occur in many patients without renal artery stenosis after unexpected dehydration, especially in older patients with congestive heart failure. In both groups of patients, in the absence of preexisting chronic uremia, recovery of renal function occurred without sequelae, even after an episode of acute tubular necrosis requiring dialysis.