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At least 1,027 records · Page 57Linked to original sources
PubMed1980

Granulomatous sarcoid nephritis: a cause of multiple renal tubular abnormalities.

We report the eleventh case of granulomatous sarcoid nephritis and review the previous literature. Although not as commonly recognized as calcium nephropath, granulomatous nephritis may be an important cause of morbidity and mortality in patients with sarcoidosis. Its characteristics are similar to other tubulo-interstitial diseases. Mild to moderate albuminuria, microscopic hematuria and sterile pyuria predominate. Hypertension is usually absent and renal size is well preserved. Urinary concentration defects (including nephrogenic diabetes insipidus), renal tubular acidosis and inappropriate glucosuria may also be seen. Interstitial inflammation with non-caseating granulomas, epithelioid and multinucleated giant cells is the usual histologic picture. Intimal thickening is not infrequent and granulomas may occasionally involve the small arteries. Immunofluorescence and electron microscopic findings are non-specific.

Adolescent↗
PubMed1994

[D-lactate, D-lactic acidosis. Biochemical review of D-lactic acid metabolism and its clinical implications].

D-lactate is an intermediate of methylglyoxal metabolism and the article gives an overview of D-lactatate metabolism as well as discusses the possible pathological role of this lactate stereoisomer. The increase of D-lactate concentration in a given body fluid can be used as a diagnostic sign, especially in patients who underwent small bowel resection or bypass operation or who have infections or suffer from certain metabolic disorders. Determination of D-lactate concentration should be considered as a useful tool both in the diagnosis and in controlling of the management of infectious diseases, particularly in those when the smear was negative or when the patient has already received antibiotics. Spite of these, the clinical value of the measurement of D-lactate concentration cannot, however, be evaluated yet.

Acidosis, Lactic↗
PubMed1976

Lactic acidosis.

Many assumptions and compromises must be made in order to establish blood lactate as a reliable parameter of tissue oxygenation. One must think not only of reactions and cells as having oxidation-reduction potentials, but the concept of the redox potential of tissues, organs and even whole patients becomes applicable. Blood lactate concentrations probably are not an accurate measure of intracellular lactate. Thermodynamic equilibrium of the intracellular lactic acid dehydrogenase system cannot be assumed and, in fact, is probably not compatible with life. Clinically, however, the lactate-pyruvate system appears to establish a dynamic equilibrium that is responsive both to oxygen supply and substrate pyruvate availability. The diagnostic and prognostic values of blood lactate with both a stable and increased lactate to pyruvate ratio have been established empirically by numerous investigators. If evaluated within the constraints of available knowledge, blood lactate concentration is a valuable indicator of tissue perfusion and an effective surgical tool.

Acid-Base Equilibrium↗
PubMed1997

[Lactic acidosis].

Explore the source record for details and available documents.

Acidosis, Lactic↗
PubMed2006

Complications of brain death: frequency and impact on organ retrieval.

Brain death is associated with complex hemodynamic, endocrine, and metabolic dysfunction that can lead to major complications with the potential donor. Untreated, this can progress to cardiovascular collapse with loss of valuable organs for transplantation. We hypothesized that brain death-related complications would have no effect on the number of organs donated if an aggressive donor management protocol was in place. We identified all successful organ donations between January 2000 and December 2003 and evaluated them for brain death-associated complications (defined as vasopressor requirement, coagulopathy, diabetes insipidus, cardiac ischemia, lactic acidosis, renal failure, and acute respiratory distress syndrome) and donated organs per donor. Sixty-nine organ donors were identified. Complications identified were as follows: intravenous vasopressor requirement in 97.1 per cent, coagulopathy in 55.1 per cent, thrombocytopenia in 53.6 per cent, diabetes insipidus in 46.4 per cent, cardiac ischemia in 30.4 per cent, lactic acidosis in 24.6 per cent, renal failure in 20.3 per cent, and acute respiratory distress syndrome in 13 per cent. There was no significant effect of complications on the average number of organs harvested, with the exception of an increase in organs harvested in the presence of diabetes insipidus. With the implementation of an aggressive organ donor management protocol, these complications can be effectively managed with no impact on the number of organs harvested for transplant.

Adult↗
PubMedDate not supplied

Life threatening hyperkalemia and acidosis secondary to trimethoprim-sulfamethoxazole treatment.

We present a 77-year-old male with moderate chronic renal insufficiency from diabetic nephropathy who developed severe metabolic acidosis and life threatening hyperkalemia on treatment with regular dose of trimethoprim-sulfamethoxazole (TMP-SMZ) for urinary tract infection. The metabolic acidosis and hyperkalemia resolved upon appropriate medical intervention and discontinuation of TMP-SMZ. While hyperkalemia has commonly been reported with high dose of TMP-SMZ, severe metabolic acidosis is quite uncommon with regular dose TMP-SMZ. We emphasize that patients with renal tubular acidosis (RTA), renal insufficiency, aldosterone deficiency, old age with reduced renal mass and function, and angiotensin converting enzyme (ACE)-inhibitor therapy are at high risk of developing these severe and potentially life threatening complications.

Acidosis, Renal Tubular↗
PubMedDate not supplied

Adult respiratory distress syndrome complicating severely uncontrolled diabetes mellitus: report of nine cases and a review of the literature.

We report the occurrence of the adult respiratory distress syndrome (ARDS) in association with uncontrolled diabetes in nine patients. In reviewing the literature we found nine similar cases reported in little over a decade. In most cases no condition known to precipitate ARDS was discovered. The evidence suggests that the severely uncontrolled diabetic state in some way may initiate pathologic events leading to the capillary leak of ARDS. This description of the association of these two entities not commonly recognized as occurring simultaneously has important clinical implications: the entity should be anticipated in uncontrolled diabetic patients who present with acidosis, hypotension, hypothermia, and/or coma. The clinical or radiologic diagnosis of pneumonia or fluid overload should not be made in the uncontrolled diabetic patient in the absence of unequivocal evidence of infection or congestive heart failure. The development of dyspnea, hypoxemia, rales, or infiltrates in the otherwise routine resuscitation of these patients should lead the clinician to suspect the development of ARDS. Prompt invasive monitoring in these cases is indicated to aid in their management and may help to improve survival. We found calculation of the A-a gradient to be useful in patients with uncontrolled diabetes. Although not necessarily predictive, widened gradients were the earliest detectable abnormality found in all patients who developed ARDS.

Adult↗
PubMed2006

Metformin-associated lactic acidosis treated with continuous renal replacement therapy.

INTRODUCTION: Lactic acidosis is an infrequent complication of metformin therapy for diabetes mellitus. The presence of clinical conditions, such as renal failure, increases the risk of metformin-associated lactic acidosis (MALA). We present a case of lactic acidosis in a patient with diabetes treated with metformin, complicated by acute renal failure in preexisting chronic nephropathy. CASE SUMMARY: A 70-year-old white male, weighing 77 kg, with diabetes mellitus, coronary heart disease, congestive heart failure (New York Heart Association class III), moderate essential hypertension (stage 2), and renal dysfunction (serum urea, 90 mg/dL; serum creatinine, 1.5 mg/dL; creatinine clearance, 49.8 mL/min/1.73 m2) presented to the emergency department of the General Hospital of Rhodes (Rhodes, Greece), complaining of malaise, respiratory distress, myalgias, disorientation, abdominal discomfort, and increasing somnolence of insidious onset. The patient's regimen included isosorbide mononitrate 60 mg QD, furosemide 40 mg QD, quinapril 20 mg QD, and metformin 850 mg TID. Before this hospitalization, he had received a 2-week course of oral diclofenac sodium 25 mg TID for low back pain. Preliminary laboratory evaluation found leukocytosis (27,300/mm3), severe renal failure (serum urea, 215 mg/dL; serum creatinine, 7.4 mg/dL; calculated creatinine clearance, 10.1 mL/min/1.73 m2), and a high anion gap metabolic acidosis (pH, 6.95; anion gap, 33 mEq/L) in arterial blood gas analysis. His medical and drug history, the clinical and laboratory findings, and the determination of lactate in samples of plasma (7.8 mEq/L), aroused the suspicion of MALA. The Naranjo algorithm scores for metformin and diclofenac sodium were 6 and 7, respectively. The patient received a single session of bicarbonate-buffered continuous venovenous hemodiafiltration (CWHDF) that lasted 16 hours. Ultimately, he was stabilized, and progressive restoration of acid-base balance and renal function was observed. DISCUSSION: We suspect that lactic acidosis may have been related to the use of metformin, the presence of heart and renal failure (contributing to metformin toxicity), and previous use of diclofenac sodium. CVVHDF has an advantage over conventional intermittent hemodialysis in that it corrects acidosis and removes lactate and metformin without risk of hypernatremia or fluid overload. CONCLUSIONS: MALA should be strongly suspected in diabetic patients presenting with high anion gap metabolic acidosis and increased serum lactate level. In the case described, prompt recognition of lactic acidosis and early application of bicarbonate-buffered CVVHDF produced successful results.

Acidosis, Lactic↗
PubMed1987

Short-term diabetes increases triacylglycerol arachidonic acid content in the rat liver.

Fatty acid compositions of liver phospholipid, cholesterol ester and triacylglycerol fractions obtained from streptozotocin-induced diabetic rats were compared to those from control or from simple-acidotic rats. Significant reductions of arachidonic acid proportions in phospholipid and cholesterol ester were found on the 3rd day after the streptozotocin treatment. In triacylglycerol, arachidonic acid and the other desaturation and elongation products of linoleic acid except for gamma-linolenic acid were increased in the diabetic rats. Although essential fatty acid composition in liver phospholipid and cholesterol ester of simple-acidotic rats did not differ from control rats, dihomo-gamma-linolenic acid, arachidonic acid, adrenic acid and docosapentaenoic acid (22:5(n - 6] contents in liver TG were significantly increased over those in control rats and were similar to those in diabetic rats. These results suggest that metabolic acidosis may contribute to the fatty acid abnormalities observed in diabetic animals.

Animals↗
PubMedDate not supplied

[Cause of dehydroascorbic acid accumulation in the blood of patients with insulin-dependent diabetes mellitus].

It is known that dehydroascorbic acid (DHAA) produces a diabetogenic effect and its content in the blood increases in diabetes mellitus. It was previously established that the generation of reducing equivalents (RE) in the course of hexosemonophosphate shunt, CO2 production and SH-glutathione regeneration in erythrocytes with and without moderate and maximum oxidation load in vitro were not disturbed in diabetes. The authors have proposed a procedure to study blood and erythrocyte DHAA reductase activity in suspension in health and in insulin-dependent diabetes mellitus by means of redoxstatometry using a device of original design. A significant acceleration of RE transfer through the erythrocyte membrane was detected in diabetes. A lowered participation in this process of the AA in equilibrium DHAA "shuttle" system was recorded in the blood of patients with diabetes mellitus what was mostly expressed under the conditions of acidosis in vitro. Probably "shuttle" function in diabetes was provided by some other redox system which might be located in the plasma. The predominant functioning of this redox system and a decrease of DHAA reductase activity in diabetes resulted in the accumulation of DHAA in the blood of patients with type I diabetes mellitus.

Adult↗