scholarly journals Hypokalemia Associated with Colonic Pseudo-Obstruction (Ogilvie's Syndrome)

2015 ◽  
Vol 5 (2) ◽  
pp. 118-123 ◽  
Author(s):  
Naseem Sunnoqrot ◽  
Robert F. Reilly

We report a case of hypokalemia resulting from colonic pseudo-obstruction or Ogilvie's syndrome. Colonic pseudo-obstruction is characterized by profuse watery diarrhea that has a low sodium and high potassium concentration. It is seen in a variety of medical and surgical conditions, but its exact cause remains unknown. It is thought to result from an imbalance of sympathetic and parasympathetic input in the distal colon. The diarrhea is secretory and driven by potassium secretion rather than the inhibition of sodium reabsorption or chloride secretion, which are the most common pathophysiologic mechanisms of secretory diarrhea. Affected patients often lose >100 mmol of potassium daily. Colonic pseudo-obstruction is associated with a dramatic upregulation of the maxiK or BK potassium channel. This channel plays a prominent role in flow-mediated potassium secretion in the connecting tubule and collecting duct and is also upregulated in the distal colon in patients with advanced chronic kidney disease and end-stage renal disease. In vitro studies show that the channel is regulated by catecholamine binding to the β receptor and cyclic AMP upregulation, somatostatin and aldosterone, insights that can be used to help guide pharmacologic therapy. Nephrologists should be aware of colonic pseudo-obstruction as a cause of extrarenal potassium loss.

2016 ◽  
Vol 2016 ◽  
pp. 1-3 ◽  
Author(s):  
Pradhum Ram ◽  
Abhinav Goyal ◽  
Marvin Lu ◽  
Joshua Sloan ◽  
William McElhaugh

Ogilvie’s syndrome (OS) is a functional obstruction of the bowel due to an autonomic imbalance. It often presents with diarrhea and is associated with hypokalemia. We present a case of a 70-year-old male who developed severe abdominal distension, watery diarrhea, and persistent hypokalemia status after left hip arthroplasty after suffering from a femoral neck fracture due to a fall and was diagnosed with OS. The persistent hypokalemia was slow to improve despite aggressive repletion because of the high potassium losses in the stool. This is most likely mediated through the increased expression of BK channels in the colonic mucosa. Aldosterone is theorized to have a role in the regulation of BK channels. Spironolactone was subsequently given and resulted in marked improvement of the diarrhea and hypokalemia. Thus, this case suggests a novel therapeutic approach for the treatment of Ogilvie’s syndrome-associated diarrhea and hypokalemia.


1975 ◽  
Vol 228 (4) ◽  
pp. 1249-1261 ◽  
Author(s):  
RN Khuri ◽  
WN Strieder ◽  
G Giebisch

Potassium transport was studied across proximal and distal tubular epithelium in rats on a normal, low- and high-potassium intake during progressive loading with isotonic saline (150 mM) or a moderately hypersomotic urea (200 mM) sodium chloride (100 mM) solution. Free-flow micropuncture and recollection techniques were used during the development of diruesis and tubular fluid (TF) analyzed for inulin-14C, potassium (K) and sodium (Na). Tubular puncture sites were localized by neoprene filling and microdissection. During the large increase in tubular flow rates (10 times): 1) fractional potassium reabsorption fell along the proximal tubule, 2) TFk along the distal tubule remained constant and independent of flow rate in control and high-k rats; thus, net potassium secretion increased in proportion to and was limited by flow rate. 3) In low-K rats TF k fell; with increasing flow rates distal K secretion was not effectively stimulated. 4) Distal tubular sodium reabsorption increased in all animals with flow rate, but tubular Na-K exchange ratios varied greatly. It is suggested that whenever sodium delivery stimulates distal tubular potassium secretion it does so by 1) increasing volume distal tubular potasssium secretion and by 2) augmenting the transepithelial electrical potential difference (lumen negative).


2018 ◽  
Vol 314 (2) ◽  
pp. F251-F259 ◽  
Author(s):  
Crystal A. West ◽  
Paul A. Welling ◽  
David A. West ◽  
Richard A. Coleman ◽  
Kit-Yan Cheng ◽  
...  

Gestational potassium retention, most of which occurs during late pregnancy, is essential for fetal development. The purpose of this study was to examine mechanisms underlying changes in potassium handling by the kidney and colon in pregnancy. We found that potassium intake and renal excretion increased in late pregnancy while fecal potassium excretion remained unchanged and that pregnant rats exhibited net potassium retention. By quantitative PCR we found markedly increased H+-K+-ATPase type 2 (HKA2) mRNA expression in the cortex and outer medullary of late pregnant vs. virgin. Renal outer medullary potassium channel (ROMK) mRNA was unchanged in the cortex, but apical ROMK abundance (by immunofluorescence) was decreased in pregnant vs. virgin in the distal convoluted tubule (DCT) and connecting tubule (CNT). Big potassium-α (BKα) channel-α protein abundance in intercalated cells in the cortex and outer medullary collecting ducts (by immunohistochemistry) fell in late pregnancy. In the distal colon we found increased HKA2 mRNA and protein abundance (Western blot) and decreased BKα protein with no observed changes in mRNA. Therefore, the potassium retention of pregnancy is likely to be due to increased collecting duct potassium reabsorption (via increased HKA2), decreased potassium secretion (via decreased ROMK and BK), as well as increased colonic reabsorption via HKA2.


1982 ◽  
Vol 242 (4) ◽  
pp. F297-F312 ◽  
Author(s):  
R. L. Jamison ◽  
J. Work ◽  
J. A. Schafer

This review focuses on the hypothesis that potassium is recycled in the medulla by secretion into the pars recta or descending limb of long-looped nephrons and reabsorption from the ascending limb and/or medullary collecting duct. Evidence supporting the recycling hypothesis is summarized and the process is analyzed quantitatively by an examination of the mass flow of potassium reaching different sites along superficial and juxtamedullary nephrons and collecting tubules. From differences in potassium mass flow between sites, we have estimated the amount of potassium that must be secreted or absorbed by individual segments of the renal tubule. These rates of secretion and absorption are compared with the potassium transport characteristics of the respective segments, as assessed by isolated tubule perfusion in vitro and micropuncture in vivo. It is apparent that potassium secretion can occur passively in the pars recta and descending limb of long-looped nephrons as a consequence of the elevated potassium concentration in the medullary interstitium. At present, no active potassium absorptive mechanism has been demonstrated in any segment of the ascending limb. Due to the very high ionic permeability of the thin ascending segment and the lumen-positive transepithelial voltage in the thick ascending segment, however, considerable passive absorption likely occurs, although net potassium secretion has also been demonstrated in the cortical thick ascending limb. The high potassium concentration in the inner medullary interstitium and the difference in mass flow of potassium between the end of superficial nephrons in the cortex and the collecting ducts in the papilla, at least under certain circumstances, are best accounted for by net potassium reabsorption in the medullary collecting duct.


2013 ◽  
Vol 304 (4) ◽  
pp. F397-F402 ◽  
Author(s):  
Chih-Jen Cheng ◽  
Michel Baum ◽  
Chou-Long Huang

Kidney-specific with-no-lysine kinase 1 (KS-WNK1) is a kinase-deficient variant of WNK1 that is expressed exclusively in the kidney. It is abundantly expressed in the distal convoluted tubule (DCT) and to a lesser extent in the cortical thick ascending limb (cTAL), connecting tubule, and cortical collecting duct (CCD). KS-WNK1 inhibits Na+-K+-2Cl−- and sodium chloride cotransporter-mediated Na+ reabsorption in cTAL and DCT, respectively. Here, we investigated the role of KS-WNK1 in regulating Na+ and K+ transport in CCD using in vitro microperfusion of tubules isolated from KS-WNK1 knockout mice and control wild-type littermates. Because baseline K+ secretion and Na+ reabsorption were negligible in mouse CCD, we studied tubules isolated from mice fed a high-K+ diet for 2 wk. Compared with that in wild-type tubules, K+ secretion was reduced in KS-WNK1 knockout CCD perfused at a low luminal fluid rate of ∼1.5 nl/min. Na+ reabsorption and the lumen-negative transepithelial potential difference were also lower in the KS-WNK1 knockout CCD compared with control CCD. Increasing the perfusion rate to ∼5.5 nl/min stimulated K+ secretion in the wild-type as well as knockout CCD. The magnitudes of flow-stimulated increase in K+ secretion were similar in wild-type and knockout CCD. Maxi-K+ channel inhibitor iberiotoxin had no effect on K+ secretion when tubules were perfused at ∼1.5 nl/min, but completely abrogated the flow-dependent increase in K+ secretion at ∼5.5 nl/min. These findings support the notion that KS-WNK1 stimulates ROMK-mediated K+ secretion, but not flow-dependent K+ secretion mediated by maxi-K+ channels in CCD. In addition, KS-WNK1 plays a role in regulating Na+ transport in the CCD.


2021 ◽  
pp. 1-3
Author(s):  
Feyza Mutlay ◽  
Derya Kaya ◽  
Ahmet Turan Isik

Abstract Objective Corticobasal syndrome (CBS) is one of an atypical parkinsonian syndromes characterized by extrapyramidal features as well as cortical involvement signs. A variety of factors may lead to delirium in older adults with chronic progressive life-limiting neurological illnesses like CBS. Ogilvie's syndrome (OS) is an acute colonic pseudo-obstruction in which abdominal distension, nausea, vomiting, and constipation can be seen. We report a case of OS identified as the underlying possible cause of delirium in an 80-year-old woman with CBS. We also discuss the importance of holistic approach which is essential to manage the underlying cause and to preserve the quality of life in particular for the frail geriatric population who potentially needs palliative care or already benefits from palliative care. Method An older patient with CBS presented with symptoms similar to that of acute colonic obstruction and subsequently developed delirium. The patient was found to have colonic pseudo-obstruction (OS). Result Neostigmin infusion was therefore given to treat it and delirium was resolved. Significance of results To the best of our knowledge, clinical manifestation of delirium as OS in a patient with CBS has not been previously reported. OS may be superimposed to CBS in older patients, and OS in such patients may play a role as a precipitating factor for the development of delirium. Given the fact that CBS is progressive and rare neurodegenerative disease and almost all of these patients need palliative care, eventually, health-care professionals, especially in palliative care, should be aware of distinctive challenges of life-limiting chronic neurological illnesses, such as conditions that may lead to the development of acute colonic pseudo-obstruction because the rapid treatment of them prevents the use of potentially harmful drugs, surgical procedures, or inappropriate interventions.


2017 ◽  
Vol 99 ◽  
pp. 302-307 ◽  
Author(s):  
Jacob Januszewski ◽  
Sean K. Keem ◽  
William Smith ◽  
Joshua M. Beckman ◽  
Adam S. Kanter ◽  
...  

2020 ◽  
Vol 31 (5) ◽  
pp. 1009-1023 ◽  
Author(s):  
Ali Sassi ◽  
Yubao Wang ◽  
Alexandra Chassot ◽  
Olga Komarynets ◽  
Isabelle Roth ◽  
...  

BackgroundWater and solute transport across epithelia can occur via the transcellular or paracellular pathways. Tight junctions play a key role in mediating paracellular ion reabsorption in the kidney. In the renal collecting duct, which is a typical absorptive tight epithelium, coordination between transcellular sodium reabsorption and paracellular permeability may prevent the backflow of reabsorbed sodium to the tubular lumen along a steep electrochemical gradient.MethodsTo investigate whether transcellular sodium transport controls tight-junction composition and paracellular permeability via modulating expression of the transmembrane protein claudin-8, we used cultured mouse cortical collecting duct cells to see how overexpression or silencing of epithelial sodium channel (ENaC) subunits and claudin-8 affect paracellular permeability. We also used conditional kidney tubule–specific knockout mice lacking ENaC subunits to assess the ENaC’s effect on claudin-8 expression.ResultsOverexpression or silencing of the ENaC γ-subunit was associated with parallel and specific changes in claudin-8 abundance. Increased claudin-8 abundance was associated with a reduction in paracellular permeability to sodium, whereas decreased claudin-8 abundance was associated with the opposite effect. Claudin-8 overexpression and silencing reproduced these functional effects on paracellular ion permeability. Conditional kidney tubule–specific ENaC γ-subunit knockout mice displayed decreased claudin-8 expression, confirming the cell culture experiments' findings. Importantly, ENaC β-subunit or α-subunit silencing or kidney tubule–specific β-ENaC or α-ENaC knockout mice did not alter claudin-8 abundance.ConclusionsOur data reveal the specific coupling between ENaC γ-subunit and claudin-8 expression. This coupling may play an important role in preventing the backflow of reabsorbed solutes and water to the tubular lumen, as well as in coupling paracellular and transcellular sodium permeability.


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