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PubMed1978

[Lactacidosis in biguanide therapy: diagnosis and therapy. 4 cases compared to 179 cases in the world literature].

In 4 out of 9711 (= 1:2400) patients, lactice acidosis due to biguanides was diagnosed. Serum lactate concentration averaged 18.2 mmol/l and the pH value 6.87. All patients showed signs of renal insufficiency and three had congestive heart disease. In addition to treatment with biguanides, other factors might have contributed to the lactice acidosis in these patients: prolonged fasting, severe dehydration due to persistent vomiting, acute bronchopneumonia, and acute pyelonephritis. On addmission, two patients were in shock and all patients were semi-conscious or comatose. All patients were treated with bicarbonate and glucose/insulin. One patient was hemodialysed. Two of our four patients died. Oour four patients are compared with 179 patients in the literature with respect to mortality and prognosis of lactic acidosis due to biguanides.

Acidosis↗
PubMed1996

Impaired proteolytic activity as a potential cause of progressive renal disease.

Renal hypertrophy (an increase in cellular protein content and cellularity as well as an accumulation of extracellular matrix) is due to the imbalance between protein synthesis and degradation. Proteolytic activity in the kidney plays an important role in maintaining this balance. Impaired renal proteolytic activity caused by such factors as high protein intake, metabolic acidosis, angiotensin II and transforming growth factor-beta 1 in vivo and in vitro may result in decreased protein degradation and subsequent induction of cellular hypertrophy, even in the absence of increased protein synthesis.

Acidosis↗
PubMed1997

Drainage of the exocrine pancreas in clinical transplantation: comparison of bladder versus enteric drainage in a consecutive series.

The purpose of this study was to define the incidence of urologic and metabolic complications after simultaneous kidney/pancreas transplantation (SKPT) with bladder drainage (BD). Review of 55 SKPT with BD performed between 1989 and 1995 demonstrated patient, kidney, and pancreas survival rates of 95%, 89%, and 78%, respectively, with a mean follow-up of 41 months (range 12-78 months). Over this follow-up period 78% of these patients experienced a urinary tract infection, 27% had hematuria, and 38% had at least one hospital admission for dehydration. Recent experience with primary enteric drainage of the exocrine secretions of the transplanted pancreas (n = 11) has demonstrated the total absence of these complications (follow-up range 2-12 months). These results suggest the value of continuous re-evaluation of surgical techniques as the care of transplant patients evolve.

Acidosis↗
PubMed1999

Functional and morphological abnormalities of mitochondria harbouring the tRNA(Leu)(UUR) mutation in mitochondrial DNA derived from patients with maternally inherited diabetes and deafness (MIDD) and progressive kidney disease.

AIMS/HYPOTHESIS: An A to G transition at nucleotide position 3243 in the mitochondrial tRNA Leu(UUR) gene has been identified in patients with maternally inherited diabetes and deafness, as well as in patients with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes, chronic progressive external ophpthalmoplegia, cardiomyopathy and progressive kidney disease. Variations in the mitochondrial DNA haplotype as well as differences in the degree and distribution of heteroplasmy in a certain tissue are factors that may contribute to the variety in phenotypical expression of the 3243 tRNA(Leu)(UUR) mutation. We have done morphological and functional experiments on mitochondria carrying the 3243 mutation derived from patients with either maternally inherited diabetes and deafness or progressive kidney disease to prove the pathogenicity of the 3243 mutation and to examine whether the mtDNA haplotype modulates the pathobiochemistry of this mutation. METHODS: We constructed clonal cell lines that contain predominantly mutated or exclusively wild-type mtDNA with a distinct mtDNA haplotype by the methodology of mitochondria-mediated transformation. Cells lacking mitochondrial DNA (rho(o)) were used as recipients and donor mitochondria were derived from fibroblasts of a patient with either maternally inherited diabetes and deafness or progressive kidney disease. The fibroblasts from these clinically distinct patients carry different mitochondrial DNA haplotypes with the 3243 mutation in heteroplasmic form. RESULTS: Heteroplasmy in the clonal cybrid cells ranged from 0 to 100%, reflecting the heterogeneity of the mitochondrial donor cell. Cybrid cells containing predominantly mutant mitochondrial DNA showed lactic acidosis, poor respiration and marked defects in mitochondrial morphology and respiratory chain complex I and IV activities. No differences were observed in the extent of the mitochondrial dysfunction between the mutant cells derived from the two donors. CONCLUSION/INTERPRETATION: These results provide evidence for a pathogenic effect of the tRNA(Leu)(UUR) mutation in maternally inherited diabetes and deafness and progressive kidney disease, and show no evidence of a contribution of the mitochondrial DNA haplotype as a modulating the biochemical expression of the mutation.

Cell Line↗
PubMed2003

Regulation of bone cell function by acid-base balance.

Bone growth and turnover results from the coordinated activities of two key cell types. Bone matrix is deposited and mineralised by osteoblasts and it is resorbed by osteoclasts, multinucleate cells that excavate pits on bone surfaces. It has been known since the early 20th century that systemic acidosis causes depletion of the skeleton, an effect assumed to result from physico-chemical dissolution of bone mineral. However, our own work has shown that resorption pit formation by cultured osteoclasts was absolutely dependent on extracellular acidification; these cells are inactive at pH levels above about 7.3 and show maximum stimulation at a pH of about 6.9. Bone resorption is most sensitive to changes in H+ concentration at a pH of about 7.1 (which may be close to the interstitial pH in bone). In this region pH shifts of < 0.05 units can cause a doubling or halving of pit formation. In whole-bone cultures, chronic HCO3- acidosis results in similar stimulations of osteoclast-mediated Ca2+ release, with a negligible physico-chemical component. In vivo, severe systemic acidosis (pH change of about -0.05 to -0.20) often results from renal disease; milder chronic acidosis (pH change of about -0.02 to -0.05) can be caused by excessive protein intake, acid feeding, prolonged exercise, ageing, airway diseases or the menopause. Acidosis can also occur locally as a result of inflammation, infection, wounds, tumours or diabetic ischaemia. Cell function, including that of osteoblasts, is normally impaired by acid; the unusual stimulatory effect of acid on osteoclasts may represent a primitive 'fail-safe' that evolved with terrestrial vertebrates to correct systemic acidosis by ensuring release of alkaline bone mineral when the lungs and kidneys are unable to remove sufficient H+ equivalent. The present results suggest that even subtle chronic acidosis could be sufficient to cause appreciable bone loss over time.

Acid-Base Equilibrium↗
PubMed1983

Glutamine synthetase activity of muscle in acidosis.

Metabolic acidosis stimulates the rate of glutamine release from muscle, and this in turn is used by the kidney in acid-base balance. NH4Cl, HCl or diabetic ketoacidosis increases the maximum activity of glutamine synthetase in skeletal muscle. Starvation and administration of adrenal steroids also increase the activity of the enzyme in muscle.

Acidosis↗