- Absence of renal enlargement in fructose-fed proximal-tubule-select insulin receptor (IR), insulin-like-growth factor receptor (IGF1R) double knockout mice. [Journal Article]
- PRPhysiol Rep 2016; 4(23)
- The major site of fructose metabolism in the kidney is the proximal tubule (PT). To test whether insulin and/or IGF1 signaling in the PT is involved in renal structural/functional responses to dietar...
The major site of fructose metabolism in the kidney is the proximal tubule (PT). To test whether insulin and/or IGF1 signaling in the PT is involved in renal structural/functional responses to dietary fructose, we bred mice with dual knockout (KO) of the insulin receptor (IR) and the IGF1 receptor (IGF1R) in PT by Cre-lox recombination, using a γ-glutamyl transferase promoter. KO mice had slightly (~10%) reduced body and kidney weights, as well as, a reduction in mean protein-to-DNA ratio in kidney cortex suggesting smaller cell size. Under control diet, IR and IGF1R protein band densities were 30-50% (P < 0.05) lower than WT, and the relative difference was greater in male animals. Male, but not female KO, also had significantly reduced band densities for Akt (protein kinase B), phosphorylated Akt(T308) and IR(Y)(1162/1163) A high-fructose diet (1-month) led to a significant increase in kidney weight in WT males (12%), but not in KO males or in either genotype of female mice. Kidney enlargement in the WT males was accompanied by a small, insignificant fall in protein-to-DNA ratio, supporting hyperplasia rather than hypertrophy. Fructose feeding of male WT mice led to significantly higher sodium bicarbonate exchanger (NBCe1), sodium hydrogen exchanger (NHE3), sodium phosphate co-transporter (NaPi-2), and transforming growth factor-β (TGF-β) abundances, as compared to male KO, suggesting elevated transport capacity and an early feature of fibrosis may have accompanied the renal enlargement. Overall, IR and/or IGF1R appear to have a role in PT cell size and enlargement in response to high-fructose diet.
- Failure to thrive and nephrocalcinosis due to distal renal tubular acidosis: A rare presentation of pediatric lupus nephritis. [Case Reports]
- SJSaudi J Kidney Dis Transpl 2016 Nov-Dec; 27(6):1239-1241
- A 9-year-old female child was initially diagnosed of having nephrocalcinosis with distal renal tubular acidosis (dRTA) while investigating for short stature. She later on developed features of nephro...
A 9-year-old female child was initially diagnosed of having nephrocalcinosis with distal renal tubular acidosis (dRTA) while investigating for short stature. She later on developed features of nephrotic syndrome (NS) while on treatment for RTA. Investigation for the cause of NS revealed very strong serological evidence in favor of systemic lupus erythematosus (SLE). Histopathological confirmation could not be done due to bilateral severely contracted kidneys. There are a few case reports of dRTA as the presentation of SLE, but nephrocalcinosis with dRTA with subsequent manifestation of SLE has hitherto not been reported in literature.
- Distal Renal Tubular Acidosis Associated with Celiac Disease and Thyroiditis. [Journal Article]
- IPIndian Pediatr 2016 Nov 15; 53(11):1013-1014
- Association of distal renal tubular acidosis (RTA) with autoimmune diseases is extremely rare in children.
Association of distal renal tubular acidosis (RTA) with autoimmune diseases is extremely rare in children.
- Functional and structural abnormalities of the kidney and urinary tract in severely malnourished children - A hospital based study. [Journal Article]
- PJPak J Med Sci 2016 Sep-Oct; 32(5):1135-1140
- CONCLUSIONS: A high frequency of functional abnormalities and noticeable proportion of structural abnormalities of urinary tract were detected in children with SAM. Current finding suggest that multicenter study at national level may be undertaken to generate better data about prevalence of renal diseases in SAM.
- Nucleotide Analogue-Related Proximal Renal Tubular Dysfunction during Long-Term Treatment of Chronic Hepatitis B: A Cross-Sectional Study. [Journal Article]
- GRGastroenterol Res Pract 2016; 2016:2952635
- Background. There have been few reports of nucleotide analogue-related renal tubular dysfunction (RTD) in CHB patients. We assessed the prevalence and presentation of nucleotide analogue-related prox...
Background. There have been few reports of nucleotide analogue-related renal tubular dysfunction (RTD) in CHB patients. We assessed the prevalence and presentation of nucleotide analogue-related proximal RTD. Methods. A cross-sectional study was performed in CHB patients taking nucleotide analogues. Inclusion criteria were patients who were on adefovir or tenofovir as mono- or add-on therapy with lamivudine (LAM) >1 year. Serum and urine were collected. Fractional excretion of phosphate (FEPO4), uric acid (FEUA), and potassium was calculated. Renal losses were defined based on the criteria: protein (24-hour urine protein >150 mg), glucose (glycosuria with normoglycemia), phosphate (FEPO4 >18%), uric acid (FEUA >15%), potassium (renal potassium losses with hypokalemia), and bicarbonate (normal gap acidosis). Subclinical and overt proximal RTD were defined when 2 and ≥3 criteria presented. Results. Ninety-two patients were enrolled. The mean duration of nucleotide analogue taking was 55.1 ± 29.6 months. Proximal RTD was found in 24 (26.1%) patients (subclinical 15 (16.3%) and overt 9 (9.8%)). The severity of RTD was associated with the duration of nucleotide analogue (P = 0.01). Conclusions. The prevalence of proximal RTD in CHB patients taking nucleotide analogues was 26%. The severity of RTD was associated with the treatment duration. Comprehensive testing is necessary for early detecting nucleotide analogue-related nephrotoxicity.
- Distal renal tubular acidosis without renal impairment after use of tenofovir: a case report. [Journal Article]
- BPBMC Pharmacol Toxicol 2016 Nov 21; 17(1):52
- CONCLUSIONS: Distal renal tubular acidosis caused by tenofovir, without renal impairment is very rare. Since causes of nausea and vomiting among HIV/AIDS patients are very diverse, awareness of this phenomenon is useful in diagnosing and managing the problem.
- Primary Sjogren's syndrome presenting as hypokalemic paralysis: A case series. [Case Reports]
- JPJ Postgrad Med 2016 Nov 16
- Primary Sjögren's syndrome (pSS) primarily involves exocrine glands, and renal tubular acidosis (RTA) is seen in one-third of the cases. RTA with hypokalemic paralysis as a presenting feature of pSS ...
Primary Sjögren's syndrome (pSS) primarily involves exocrine glands, and renal tubular acidosis (RTA) is seen in one-third of the cases. RTA with hypokalemic paralysis as a presenting feature of pSS is described in few case reports in literature. We report 13 cases who presented as hypokalemic paralysis, and on evaluation were diagnosed to be pSS, as per the diagnostic criteria laid by the Sjφgren's International Collaborative Clinical Alliance (2012). All patients were female, with a mean age at presentation being 33.1 ± 8.22 years (range, 25-48 years). Eleven patients had a complete distal RTA and two patients had incomplete distal RTA at the time of presentation. 62% (8/13) of patients had no signs and symptoms of exocrine gland involvement. All the cases were managed with oral alkali therapy, and six patients received additional immunomodulating agents. No improvement in renal tubular dysfunction (in the form of a reduction in the alkali dose) after immunomodulating therapy was observed over a mean follow-up of 2.8 years. Renal tubular dysfunction can be the presenting manifestation of pSS. It is important to consider the possible presence of this disorder in adults with otherwise unexplained distal RTA or hypokalemia.
- Ethylene Glycol Poisoning: An Unusual Cause of Altered Mental Status and the Lessons Learned from Management of the Disease in the Acute Setting. [Journal Article]
- CRCase Rep Crit Care 2016; 2016:9157393
- Ethylene glycol is found in many household products and is a common toxic ingestion. Acute ingestions present with altered sensorium and an osmolal gap. The true toxicity of ethylene glycol is mediat...
Ethylene glycol is found in many household products and is a common toxic ingestion. Acute ingestions present with altered sensorium and an osmolal gap. The true toxicity of ethylene glycol is mediated by its metabolites, which are responsible for the increased anion gap metabolic acidosis, renal tubular damage, and crystalluria seen later in ingestions. Early intervention is key; however, diagnosis is often delayed, especially in elderly patients presenting with altered mental status. There are several laboratory tests which can be exploited for the diagnosis, quantification of ingestion, and monitoring of treatment, including the lactate and osmolal gaps. As methods of direct measurement of ethylene glycol are often not readily available, it is important to have a high degree of suspicion based on these indirect laboratory findings. Mainstay of treatment is bicarbonate, fomepizole or ethanol, and, often, hemodialysis. A validated equation can be used to estimate necessary duration of hemodialysis, and even if direct measurements of ethylene glycol are not available, monitoring for the closure of the anion, lactate, and osmolal gaps can guide treatment. We present the case of an elderly male with altered mental status, acute kidney injury, elevated anion gap metabolic acidosis, and profound lactate and osmolal gaps.
- Genetic defects underlying renal stone disease. [Review]
- IJInt J Surg 2016 Nov 10
- Renal stones are common and are usually secondary to risk factors affecting the solubility of substances in the urinary tract. Primary, that is genetic, causes are rare but nevertheless are important...
Renal stones are common and are usually secondary to risk factors affecting the solubility of substances in the urinary tract. Primary, that is genetic, causes are rare but nevertheless are important to recognise so that appropriate treatments can be instigated and the risks to other family members acknowledged. A brief overview of the investigation of renal stones from a biochemical point of view is presented with emphasis on the problems that can arise. The genetic basis of renal stone disease caused by (i) derangement of a metabolic pathway, (ii) diversion to an insoluble product, (iii) failure of transport and (iv) renal tubular acidosis is described by reference to the disorders of adenine phosphoribosyl transferase (APRT) deficiency, primary hyperoxaluria, cystinuria and autosomal dominant distal renal tubular acidosis.
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- Hypokalemia and suspected renal tubular acidosis associated with topical carbonic anhydrase inhibitor therapy in a cat. [Journal Article]
- JVJ Vet Emerg Crit Care (San Antonio) 2016; 26(6):870-874
- CONCLUSIONS: This is the first report of hypokalemia and metabolic acidosis associated with topical CAI therapy in a cat.