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Renal AND Renal tubular acidosis [keywords]
- Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis. [REVIEW]
- ScientificWorldJournal 2014.:627673.
Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.
- Renal tubular acidosis: an uncommon cause of bad obstetric history. [Journal Article]
- J Obstet Gynaecol India 2014 Dec; 64(Suppl 1):34-5.
- Prevalence and European AIDS Clinical Society (EACS) criteria evaluation for proximal renal tubular dysfunction diagnosis in patients under antiretroviral therapy in routine setting. [Journal Article]
- J Int AIDS Soc 2014; 17(4 Suppl 3):19564.
Tenofovir (TDF) is an antiretroviral drug often used in combination regimen in HIV-positive patients. Adverse effects affecting kidneys consist in an increase or a new onset proteinuria, a decrease of glomerular filtration rate (GFR), and/or a proximal renal tubular dysfunction (PRTD) that rarely leads to Fanconi's syndrome. EACS guidelines propose to screen PRTD in patients with chronic renal insufficiency, with a sudden decrease of eGFR, with hypophosphataemia (if non-renal causes such as vitamin D deficiency are excluded) and with a new onset proteinuria. We aim to evaluate the prevalence of PRTD by comparing the group of patients under TDF to the group free of TDF, in our cohort of 300 patients. We also aim to evaluate the accuracy of EACS criteria for screening PRTD in routine settings and to assess the utility of urinary samples in PRTD diagnosis.During two consecutive years, we collected annually blood and urine samples at the same time in our outpatient clinic. We assessed kidney function, plasma levels and fractional excretion of phosphate, uric acid, potassium, plasma glucose and proteinuria. PRTD was defined by the presence of at least two out of the five following criteria: fractional excretion (FE) of phosphate >20% (or >10% when serum phosphate <0.8 mmol/L), non-diabetic glycosuria (positive urine glucose with plasma glucose <70 mg/dL), renal tubular acidosis (urinary pH >5.5 and serum bicarbonate <21 mmol/L), uric acid FE >10% or potassium FE >10%. After the first year, patients with TDF regimen who were diagnosed with PRTD were shifted to TDF-free regimen and included again in the study.For PRTD (first line), they are expressed in number of diagnoses/total number of patients in this group. The second line resumes the number of PRTD diagnose patients who should have been screened according to EACS criteria.PRTD screening according to EACS criteria is not sufficient to diagnose every case, especially minor PRTD, mainly because the prevalence is low and its diagnosis remains difficult in routine settings. We recommend performing a urine test including proteinuria every year for patients undergoing TDF treatment. The next step will be to follow PRTD patients to evaluate the time laps until full recovery after TDF shift.
- Effect of Mineralocorticoids on Acid-Base Balance. [JOURNAL ARTICLE]
- Nephron Physiol 2014 Nov 6.
Aldosterone is classically associated with the regulation of salt and potassium homeostasis but has also profound effects on acid-base balance. During acidosis, circulating aldosterone levels are increased and the hormone acts in concert with angiotensin II and other factors to stimulate renal acid excretion. Pharmacological blockade of aldosterone action as well as inherited or acquired syndromes of impaired aldosterone release or action impair the renal response to acid loading and cause hyperkalemic renal tubular acidosis. The mineralocorticoid receptor (MR) mediating the genomic effects of aldosterone is expressed in all cells of the distal nephron including all subtypes of intercalated cells. In acid-secretory type A intercalated cells, aldosterone stimulates proton secretion into urine, whereas in non-type A intercalated cells, aldosterone increases the activity of the luminal anion exchanger pendrin stimulating bicarbonate secretion and chloride reabsorption. Aldosterone has also stimulatory effects on proton secretion that may be mediated by a non-genomic pathway. In addition, aldosterone indirectly stimulates renal acid excretion by enhancing sodium reabsorption through the epithelial sodium channel ENaC. Increased sodium reabsorption enhances the lumen-negative transepithelial voltage that facilitates proton secretion by neighboring intercalated cells. This indirect coupling of sodium reabsorption and proton secretion is thought to underlie the fludrocortisone-furosemide test for maximal urinary acidification in patients with suspected distal renal tubular acidosis. In patients with CKD, acidosis-induced aldosterone may contribute to progression of kidney disease. In summary, aldosterone is a powerful regulator of renal acid excretion required for normal acid-base balance. © 2014 S. Karger AG, Basel.
- Drug-induced acid-base disorders. [JOURNAL ARTICLE]
- Pediatr Nephrol 2014 Nov 5.
The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal anti-inflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk-alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g., anesthetics, sedatives) or hyperventilation (e.g., salicylates, epinephrine, nicotine).
- Obstetric anesthesia considerations in Kearns-Sayre syndrome: a case report. [Journal Article]
- Korean J Anesthesiol 2014 Oct; 67(4):283-6.
Kearns-Sayre syndrome (KSS) is a rare mitochondrial myopathy that usually develops before 20 years of age. It demonstrates multisystemic involvement with a triad of cardinal features: progressive ophthalmoplegia, pigmentary retinopathy, and cardiac conduction abnormalities. In addition, patients might have cerebellar ataxia, a high content of protein in the cerebrospinal fluid, proximal myopathy, multiple endocrinopathies, and renal tubular acidosis. We herein report the successful obstetric analgesic and anesthetic management of a 28-year-old parturient patient with KSS who required labor analgesia and proceeded to deliver by cesarean section. We extrapolate that regional analgesia/anesthesia might be beneficial for reducing the metabolic demands associated with the stress and pain of labor in patients with KSS. Efficient postoperative analgesia should be provided to decrease oxygen requirements.
- Serum cystatin C is not an appropriate marker for kidney involvement in patients with primary Sjögren's syndrome. [JOURNAL ARTICLE]
- Int J Rheum Dis 2014 Nov 4.
We aimed to investigate serum cystatin C (cysC) levels in primary Sjögren's syndrome (pSS) patients, and evaluate its correlation with renal involment.Eighty-six pSS patients and 65 age- and gender-matched healthy controls were enrolled into the study. Serum cysC, urea, serum creatinine (SCr), creatinine clearance (CrCl), glomerular filtration rates (GFR), Na, K, Mg, Ca, uric acid, P, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), anti-Ro/SS-A, anti-La/SS-B, antinuclear antibodies, 24-h urinary poteinuria and microalbuminuria were evaluated.Mean serum cysC levels did not differ between the patients and healthy controls (P > 0.05). Nine patients with pSS had proteinuria over 150 mg (and microalbuminuria over 30 mg) per 24 h. In patients with proteinuria, serum cysC levels correlated with serum K (r = 0.279, P = 0.024), ESR (r = 0.405, P = 0.001) and the disease duration (r = 0.235, P = 0.04), respectively. Patients with positive anti-Ro/SS-A and anti-La/SS-B antibodies had higher SCr levels compared to those with negative serology (r = 0.292, P = 0.009, and r = 0.259, P = 0.022, respectively). Nine patients with proteinuria and anti-Ro/SS-A, anti-La/SS-B positivity tended to have lower K and Mg levels which suggests subclinical renal tubular acidosis.There were no associations between serum cysC levels and renal involvement in patients with pSS. However, in patients with proteinuria, serum cysC levels were correlated with acute-phase reactants, suggesting an association with disease activity in terms of degree of inflammation.
- Wilson's disease: An endocrine revelation. [Journal Article]
- Indian J Endocrinol Metab 2014 Nov; 18(6):855-7.
Wilson's disease is an inherited disorder of copper metabolism. The affected patients, who otherwise have a near normal life span, may often suffer from some potentially treatable and under recognized endocrine disorders that may hinder their quality of life. We explored previously published literature on the various endocrine aspects of this disease with their probable underlying mechanisms, highlighting the universal need of research in this area.
- Prevalence of distal renal tubular acidosis in primary Sjögren's syndrome. [JOURNAL ARTICLE]
- Rheumatology (Oxford) 2014 Oct 29.
Our objectives were to analyse the prevalence of distal renal tubular acidosis (dRTA) in primary SS (pSS) and to compare a novel urinary acidification test with furosemide and fludrocortisone (FF) with the gold standard ammonium chloride (NH4Cl) to detect dRTA.Urinary acidification was assessed in 57 pSS patients using NH4Cl and FF. A urinary acidification defect was defined as an inability to reach a urinary pH of <5.3 after NH4Cl.The prevalence of complete dRTA (urinary acidification defect with acidosis) was 5% (3/57). All three patients had positive SSA/Ro and SSB/La autoantibodies and impaired kidney function. The prevalence of incomplete dRTA (urinary acidification defect without acidosis) was 25% (14/57). Compared with patients without dRTA, patients with incomplete dRTA had significantly lower venous pH and serum bicarbonate and higher urinary pH. SSB/La antibodies were more prevalent in the dRTA groups (P < 0.05). Compared with NH4Cl, the positive and negative predictive values of FF were 46% and 82%, respectively. Vomiting occurred more often during the urinary acidification test with NH4Cl than with FF (9 vs 0, P < 0.05).Incomplete dRTA is common in pSS and causes mild acidaemia and higher urinary pH, which may contribute to bone demineralization and kidney stone formation. FF cannot replace NH4Cl in testing urinary acidification in pSS, but may be considered as a screening tool, given its reasonable negative predictive value and better tolerability.
- Familial mixed nephrocalcinosis as a cause of chronic kidney failure: two case reports. [Journal Article]
- J Med Case Rep 2014; 8(1):355.
Nephrocalcinosis consists of the deposition of calcium salts in the renal parenchyma and is considered the mixed form when it involves the renal cortex and medulla. The main etiological agents of this condition are primary hyperparathyroidism, renal tubular acidosis, medullary sponge kidney, hyperoxaluria and taking certain drugs. These factors can lead to hypercalcemia and/or hypercalciuria, which can give rise to nephrocalcinosis.Patient 1 was a 48-year-old Caucasian woman with a history of bilateral nephrocalcinosis causing chronic kidney failure. Imaging examinations (X-ray, ultrasound and computed tomography of the abdomen) revealed extensive calcium deposits in the renal parenchyma, indicating nephrocalcinosis as the causal factor of the disease. Patient 2 is the 45-year-old brother of patient 1. He exhibited an advanced stage of chronic kidney failure. As nephrocalcinosis is considered to have a genetic component, a family investigation revealed this condition in patient 2.Nephrocalcinosis may be detected incidentally through diagnostic imaging studies. Whenever possible, treatment should include the base disease that caused the appearance of the calcification, as the precise etiological determination is extremely important.