Man Oh - Academia.edu (original) (raw)

Papers by Man Oh

Seminars in Dialysis, Oct 1, 2007

Seminars in Dialysis, Apr 1, 2019

The dialysate alkali used in hemodialysis to replace low body alkali levels in end stage renal di... more The dialysate alkali used in hemodialysis to replace low body alkali levels in end stage renal disease (ESRD) patients has changed over time from bicarbonate to acetate and finally back to bicarbonate with a small addition of acetate. The ideal way to replace alkali in dialysis patients remains uncertain. Elsewhere in this issue of the journal, Sargent and Gennari, who have contributed greatly to our understanding of dialysis and acid-base kinetics, suggest that decreasing the currently used concentration of bicarbonate while increasing concentration of acetate in the dialysate may be a much more physiological approach to alkali delivery during hemodialysis.

Nephron Clinical Practice, 1996

Urea absorption in the inner medullary collecting duct provides a mechanism to elevate the concen... more Urea absorption in the inner medullary collecting duct provides a mechanism to elevate the concentration of urea in the papillary interstitial fluid and thereby permit the excretion of urea with as little water as possible. Urea reabsorption may have another important effect - to aid in the excretion of potassium (K). K excretion depends on two processes: first, factors such as aldosterone which cause the concentration of K in the luminal fluid of the cortical distal nephron to be high and, second, factors which augment the flow rate through those nephron segments. Since, the osmolality of the luminal fluid in the cortical collecting duct (CCD) and plasma are equal when antidiuretic hormone acts, the flow rate in the CCD is dependent on solute delivery. Urea is a major solute in the lumen of the CCD and thereby plays an important role in maintaining the CCD flow rate. Since urea and K are often found in the same foods, having urea help the excretion of K is potentially advantageous. If the excretion of urea was low, the flow rate in the terminal CCD would decline. In this circumstance, the luminal K concentration would have to rise in proportion to the fall in flow rate or there would be a diminished rate of excretion of K and, possibly, hyperkalemia.

Nephron Clinical Practice, 1994

Journal of The American Society of Nephrology, May 1, 2021

Two papers, one in 1986 and another one in 1988, reported a strong inverse correlation between ur... more Two papers, one in 1986 and another one in 1988, reported a strong inverse correlation between urinary anion gap (UAG) and urine ammonia excretion (UNH4) in patients with metabolic acidosis and postulated that UAG could be used as an indirect measure of UNH4. This postulation has persisted until now and is widely accepted. In this review, we discuss factors regulating UAG and examine published evidence to uncover errors in the postulate and the design of the original studies. The essential fact is that, in the steady state, UAG reflects intake of Na, K, and Cl. Discrepancy between intake and urinary output of these electrolytes (i.e., UAG) indicates selective extrarenal loss of these electrolytes or nonsteady state. UNH4 excretion, which depends, in the absence of renal dysfunction, mainly on the daily acid load, has no consistent relationship to UAG either theoretically or in reality. Any correlation between UAG and UNH4, when observed, was a fortuitous correlation and cannot be extrapolated to other situations. Furthermore, the normal value of UAG has greatly increased over the past few decades, mainly due to increases in dietary intake of potassium and widespread use of sodium salts with anions other than chloride as food additives. The higher normal values of UAG must be taken into consideration in interpreting UAG.

The American Journal of the Medical Sciences, Feb 1, 2007

Hyponatremia, the most common electrolyte disorder in hospitalized patients, has been associated ... more Hyponatremia, the most common electrolyte disorder in hospitalized patients, has been associated with high rate of mortality among both this population and nonhospitalized patients. This review describes briefly the classification and pathogenesis of hyponatremia, and, in greater detail, the management of hyponatremia with a particular emphasis on the clinical pharmacology of arginine vasopressin (AVP) antagonists. This review includes more in-depth discussion on the pharmacology of conivaptan, an AVP antagonist recently approved by the United States Food and Drug Administration. KEY INDEXING TERMS: Hyponatremia; Management of hyponatremia; AVP-receptor antagonists. [Am J Med Sci 2007;333(2):101-105.]

PubMed, Dec 1, 1998

Our purpose is to review the topic of acute postoperative hyponatremia by focusing on pertinent a... more Our purpose is to review the topic of acute postoperative hyponatremia by focusing on pertinent aspects of the physiology of water and solute excretion. Four areas will be highlighted: an examination of the source of addition of electrolyte-free water, an exploration of the basis for the very large natriuresis that occurs during cerebral salt wasting following neurosurgery, possible reasons to explain why acute postoperative hyponatremia may pose a greater risk for young women [Ayus and Arieff 1996, Ayus et al. 1992, Arieff 1986, Wijdick et al. 1991], and issues related to treatment of acute hyponatremia.

Nephron, 2002

The urine anion gap is measured as the sum of urine Na&amp;amp;plus; and K&amp;am... more The urine anion gap is measured as the sum of urine Na&amp;amp;plus; and K&amp;amp;plus; minus urine Cl–, and the normal value is about 40 mEq/24 h. For calculation of the urine anion gap 24-hour excretion rates rather than urinary concentrations are used because the latter vary greatly with water intake and are, therefore, not as reliable as the former. The

Nephron, 1975

A group of patients whose dietary potassium was unrestricted and who received 12-18 h of Kiil dia... more A group of patients whose dietary potassium was unrestricted and who received 12-18 h of Kiil dialysis twice weekly against a bath containing no potassium, had body potassium concentrations (total body potassium/intracellular volume) of 7.6% lower than normal. Despite marked hypokalemia at the end of dialysis, suprisingly few electrocardiographic changes were seen. Another group of subjects, dialyzed fro 5-6 h thrice weekly against a bath containing 1 mEq/liter of potassium in a Dow dialyzer, showed more marked electrocardiographic abnormalities despite smaller alterations in transmembrane potassium gradients. Rapidity of establishment of potassium gradients is important as well as magnitude. The following changes occur in a single dialysis: 100 mEq of cell potassium and 20 mEq of extracellular potassium leave the body; 100 mEq of extracellular sodium enter the cells and 415 mEq of extracellular sodium leave the body; 3.5 liters of water leave the extracellular fluid, 2.5 liters into the bath and 1 liter into the cells.

Metabolism-clinical and Experimental, Feb 1, 1980

Nephron, 1999

... Cerebral Salt-Wasting Syndrome We Need Better Proof of Its Existence Man S. Oh, Hugh J. Carro... more ... Cerebral Salt-Wasting Syndrome We Need Better Proof of Its Existence Man S. Oh, Hugh J. Carroll Department of Medicine, State University of New York, Health Science Center at Brooklyn, NY, USA. ... (2) Extracellular volume (ECV): There is a great deal of individual variation in ...

Critical Care Medicine, 1992

ObjectiveDiscussion of abnormal plasma sodium concentrations with an emphasis on the pathogenesis... more ObjectiveDiscussion of abnormal plasma sodium concentrations with an emphasis on the pathogenesis, diagnosis, and treatment. Data SourcesRelevant literature in the English language and the authors' clinical experience. Study SelectionNo special study has been carried out for the present discussion. Data ExtractionThe information from the literature and the data from the authors' clinical experience have been used to illustrate important points in the discussion. Data SynthesisA most important aspect in the approach to hypernatremia is determination of the mechanism responsible for impaired water intake. Various mechanisms of abnormal water loss can be determined from measurement of urine osmolality. Hypernatremia is treated by water replacement and measures to reduce abnormal water loss. In most instances, hyponatremia is caused by inappropriate concentration of urine because of either appropriate or inappropriate antidiuretic hormone secretion. The determination of appropriateness of antidiuretic hormone secretion requires the assessment of effective arterial volume. Treatment depends on the pathogenetic mechanism. ConclusionsAbnormal plasma sodium concentration results from abnormal water intake or water output. Treatment is guided by determining the pathogenetic mechanism. (Crit Care Med 1992; 20:94)

Case reports in nephrology, Nov 23, 2022

Ogilvie's syndrome, also known as acute colonic pseudo-obstruction (ACPO), is a rare, nonobstruct... more Ogilvie's syndrome, also known as acute colonic pseudo-obstruction (ACPO), is a rare, nonobstructive dilation of the colon of unclear etiology. We present the case of a patient who presented with Ogilvie's syndrome and signifcant hypokalemia due to colonic loss despite repletion. Tis case report demonstrates the difculty in diagnosis, treatment, and outcome.

Nephron Clinical Practice, 2002

Nephron, 1978

15 patients who had benign, uncomplicated essential hypertension, were treated with chlorthiazide... more 15 patients who had benign, uncomplicated essential hypertension, were treated with chlorthiazide (500 mg twice a day) with or without propranolol (10--20 mg 4 times a day), and the effect of the treatment on plasma renin activity (PRA), urinary aldosterone excretion, total body potassium (TBK) and plasma sodium and potassium was evaluated. TBK depletion was significant mathematically (more than 5% of TBK lost) in 7 patients, but not significant physiologically (less than 15% of TBK lost) in any except in one, who may have had other reason for TBK depletion. Although propranolol prevented the increase in PRA and aldosterone excretion, it did not prevent the modest TBK depletion. Dietary potassium intake may have some importance in the maintenance of normal body potassium during chronic treatment with thiazides for hypertension.

Contributions To Nephrology, Apr 16, 2015

Kidney International, 2012