Effects of potassium on ammonia transport by medullary thick ascending limb of the rat.

Good, David W.

doi:10.1172/jci113213

Cited by 51 publications

(22 citation statements)

References 34 publications

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“…Good has suggested that changes in luminal potassium concentration in the physiologic range may modulate ammonium transport in the thick ascending limb such that high luminal potassium concentrations inhibit ammonium ion reabsorption in this segment, thereby reducing the accumulation of total ammonia in the medulla (16). In the present study, high luminal potassium concentrations in proximal tubule segments stimulated net secretion of total ammonia into the lumen.…”

Section: Discussionsupporting

confidence: 55%

“…In fact, ammonium ions may be transported instead of potassium ion on the Na'-K' ATPase of the proximal tubule (14,15), and probably on the NaKCI cotransporter in the thick ascending limb of Henle (16). The present studies in isolated mouse proximal tubules demonstrate the influence of ambient K+ concentration on net luminal secretion of ammonia.…”

Section: Discussionmentioning

confidence: 58%

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Effect of bath and luminal potassium concentration on ammonia production and secretion by mouse proximal tubules perfused in vitro.

Nagami¹

1990

J. Clin. Invest.

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To determine the effects of acute changes in K+ concentration in vitro on ammonia production and secretion by the proximal tubule, we studied mouse S2 segments perfused with and bathed in Krebs-Ringer bicarbonate buffers containing various K+ concentrations. All bath solutions contained L-lutamine as the ammoniagenic substrate. High bath and luminal K+ concentrations (8 mM), but not high luminal K+ concentration alone, inhibited total ammonia production rates by 26%, while low bath and luminal K+ concentrations (2 mM), but not low luminal K+ concentration alone, stimulated total ammonia production rates by 33%. The stimulation of ammonia production by low bath K+ concentration was not observed when L-glutamine was added to the luminal perfusion solution. On the other hand, high luminal K+ concentration stimulated, while low luminal K+ concentration inhibited, net luminal secretion of total ammonia in a way that was: (a) independent of total ammonia production rates, (b) independent of Na'-H' exchange activity, and (c) not due to changes in transepithelial fluxes of total ammonia. These results suggest that luminal potassium concentration has a direct effect on cell-to-lumen transport of ammonia. (J. Clin. Invest. 1990. 86:32-39.)

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Section: Discussionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 58%

Effect of bath and luminal potassium concentration on ammonia production and secretion by mouse proximal tubules perfused in vitro.

Nagami¹

1990

J. Clin. Invest.

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“…Moreover, they have been shown to interact with H + -K + -ATPase and influence its activity in the rabbit gastric mucosa (16). However, the slight changes in blood K + concentrations at baseline and upon acid loading (SI Appendix, Tables S1 and S2) were unlikely to affect renal acid-base handling in mutant mice (37,38). Concomitantly, ammoniagenesis in isolated proximal tubular segments of double-mutant cortices was similar to controls.…”

Section: Discussionmentioning

confidence: 96%

Sulfatides are required for renal adaptation to chronic metabolic acidosis

Stettner

Bourgeois

Marsching

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Urinary ammonium excretion by the kidney is essential for renal excretion of sufficient amounts of protons and to maintain stable blood pH. Ammonium secretion by the collecting duct epithelia accounts for the majority of urinary ammonium; it is driven by an interstitium-to-lumen NH 3 gradient due to the accumulation of ammonium in the medullary and papillary interstitium. Here, we demonstrate that sulfatides, highly charged anionic glycosphingolipids, are important for maintaining high papillary ammonium concentration and increased urinary acid elimination during metabolic acidosis. We disrupted sulfatide synthesis by a genetic approach along the entire renal tubule. Renal sulfatide-deficient mice had lower urinary pH accompanied by lower ammonium excretion. Upon acid diet, they showed impaired ammonuria, decreased ammonium accumulation in the papilla, and chronic hyperchloremic metabolic acidosis. Expression levels of ammoniagenic enzymes and Na + -K + /NH 4 + -2Cl − cotransporter 2 were higher, and transepithelial NH 3 transport, examined by in vitro microperfusion of cortical and outer medullary collecting ducts, was unaffected in mutant mice. We therefore suggest that sulfatides act as counterions for interstitial ammonium facilitating its retention in the papilla. This study points to a seminal role of sulfatides in renal ammonium handling, urinary acidification, and acid–base homeostasis.

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“…2 Therefore, both mechanisms of RTA type 4 work together to inhibit the excretion of NH3 into the collecting duct of the kidney and subsequently inhibit the excretion of NH4+ and an acid load.…”

Section: A 67 Year-old Man With Fatiguementioning

confidence: 99%

A 67 Year-Old Man with Fatigue

Barasch¹,

Wagh²

2009

TMF

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A 67 year-old male with a past medical history of hypertension and insulin-dependent type II diabetes complicated by neuropathy, retinopathy, and chronic kidney disease presented to the hospital with a complaint of fatigue. The patient noted generalized weakness that had begun the morning of admission after two days of malaise and subjective fever. This weakness prevented him from being able to rise from a sitting position, resulting in a fall off the couch. He denied injury from this fall along with shortness of breath or chest pain, however, he did admit to two episodes of vomiting the day prior to admission.The patient was taking the following medications: furosemide, aspirin, isosorbide mononitrate, lipitor, levothyroxine, candesartan, metoprolol, clopidogrel, doxazosin, calcitriol and Insulin 70/30. Medical history included, hyperlipidemia, hypothyroidism, benign prostatic hypertrophy, stable angina, and peripheral vascular disease along with the conditions listed above. Past surgical history included 2 stents in the LAD coronary artery, vitrectomy, and transurethral resection of the prostate (TURP). Additionally, the patient noted that he lived alone after having retired from teaching and denied any drugs, smoking or alcohol.On physical exam, the patient was febrile at 102.2°F, heart rate was 99, respiratory rate was 17, and blood pressure was elevated at 183/56 mmHg. Generally, the patient was dehydrated and appeared to be somnolent but responsive to questions. Neurological exam was remarkable for generalized bilateral upper and lower extremity weakness and asterixis with no focal neurological deficits. His cranial nerves were intact. Skin exam was significant for a warm, erythematous, blanching, non-pruritic rash on the left anterior tibial surface, as well as an eschar on the 2nd toe of the left foot. The rest of physical exam was within normal limits.An arterial blood gas was performed due to his overall lethargic state and demonstrated a pH of 7.34, PCO2 34, PO2 66 and oxygen saturation of 91% on room air. His electrolytes were Na 134, K 5.3, Cl 106, HCO3 19, significant for a non-anion gap metabolic acidosis with a compensatory respiratory alkalosis. Glucose was elevated at 412mg/dl. Additional laboratory values revealed a BUN of 79 and creatinine of 3.1 (previous baseline of 2.3). Urine studies showed protein >300 mg/dl, urine pH of 5.5, urine glucose 500, and rare hyaline casts. Urine electrolytes results included Na 49, K 30.2, Cl 54, and Cr of 98.7. Lactate was within normal limits.The patient was treated acutely for dehydration and hyperglycemia with intravenous fluids and insulin. He was started on broad spectrum antibiotics for suspected cellulitis and osteomyelitis of the 2nd left toe. The combined results of the urine anion gap of + 25.2, the serum anion gap of 9, and hyperkalemia led us to a preliminary diagnosis of renal tubular acidosis type IV. Finally, the renin level returned low at 1.4 ng/ mL/hr (normal 1.9-3.7) indicating a low renin -low aldosterone as an underlying cause of the met...

show abstract

Effects of potassium on ammonia transport by medullary thick ascending limb of the rat.

Cited by 51 publications

References 34 publications

Effect of bath and luminal potassium concentration on ammonia production and secretion by mouse proximal tubules perfused in vitro.

Effect of bath and luminal potassium concentration on ammonia production and secretion by mouse proximal tubules perfused in vitro.

Sulfatides are required for renal adaptation to chronic metabolic acidosis

A 67 Year-Old Man with Fatigue

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