No abstract available.
Acidosis, Renal Tubular*

No abstract available.
Acidosis, Renal Tubular* ; Captopril*

No abstract available.
Acidosis, Renal Tubular*

No abstract available.
Acidosis, Renal Tubular* ; Arthritis, Rheumatoid* ; Sjogren's Syndrome*

No abstract available.
Acidosis, Renal Tubular* ; Lupus Erythematosus, Systemic*

No abstract available.
Acidosis, Renal Tubular* ; Humans ; Infant, Newborn*

Renal tubular acidosis is a clinical state of systemic hyperchloremic acidosis resulting from impaired urine acidification. Medullary sponge kidney is a renal parenchymal malformation characterized by cystic dilatation of the collecting ducts. Although medullary sponge kidney is a congenital disease, it is rarely identified in childhood and is usually discovered in adulthood. Medullary sponge kidney patients may have defects in urinary acidification and concentration mechanism. We experienced a case of distal renal tubular acidosis associated with medullary sponge kidney. So, we report a case of distal renal tubular acidosis associated with medullary sponge kidney with a brief review of the related literature.
Acidosis ; Acidosis, Renal Tubular* ; Dilatation ; Humans ; Medullary Sponge Kidney*

No abstract available.
Acetazolamide ; Acidosis ; Acidosis, Renal Tubular ; Hypokalemic Periodic Paralysis ; Muscle Weakness

Unlike most other inborn errors of metabolism, which require advanced and expensive diagnostic techniques and complex drug and dietary management (often not feasible in developing countries), the renal tubular acidoses may be detected and treated both easily and cheaply. Diagnostic confusion is possible as this series demonstrates due to the protean clinical manifestations. Three recent cases from Port Moresby General Hospital are described and appropriate investigations and treatment discussed.
Acidosis, Renal Tubular - diagnosis ; Acidosis, Renal Tubular - metabolism ; Child, Preschool ; Female ; Humans, Infant

To evaluate urinary acidification defect and its contribution to metabolic acidosis (MA) during hemorrhagic fever with renal syndrome (HFRS), we serially analyzed acid-base balance and urinary acidification indices in 10 HFRS patients. Data of the patients were compared with those of 8 normal volunteers (NC). MA was observed in 6 of 8 patients in the oliguric phase, 5 of 7 in the early diuretic phase, 8 of 10 in the late diuretic phase and 2 of 9 in the convalescent phase. HFRS patients with MA had a higher plasma anion gap in the oliguric and early diuretic phases than NC and a higher plasma Cl/Na ratio in the late diuretic phase than NC. As compared with acid-loaded NC, HFRS patients had a higher urine pH in the oliguric, early diuretic and late diuretic phases, a higher urine anion gap (UAG) in the oliguric and early diuretic phases and a lower urinary NH4+ excretory rate in the oliguric, early diuretic and late diuretic phases. Overt distal acidification defect was observed in 6 of 8 patients in the oliguric phase, 3 of 7 in the early diuretic phase, 5 of 10 in the late diuretic phase and none of 9 in the convalescent phase. None of the convalescent patients had latent acidification defect. In conclusion, urinary acidification defect is marked in the oliguric and diuretic phases of severe HFRS and may play a role in the development of a high anion gap (AG) metabolic acidosis in the earlier phase and hyperchloremic MA in the later phase, but rapidly recovers in the convalescent phase.
Acidosis, Renal Tubular/urine ; Acidosis, Renal Tubular/metabolism ; Hemorrhagic Fever with Renal Syndrome/urine ; Hemorrhagic Fever with Renal Syndrome/metabolism ; Human