Pravit Cadnapaphornchai
Wayne State University
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Featured researches published by Pravit Cadnapaphornchai.
The American Journal of Medicine | 1985
R. Kebler; F.D. McDonald; Pravit Cadnapaphornchai
The dynamic changes in serum phosphorus levels in 69 episodes of ketoacidosis in 48 diabetic patients were retrospectively evaluated. The mean age was 41 +/- 2 years (mean +/- SEM), and the duration of diabetes mellitus was 7 +/- 1 years. The serum phosphorus levels determined within the first six hours of admission were analyzed. Before initiation of therapy, the incidence of hyperphosphatemia was 94.7 percent. At the end of 12 hours, the mean serum phosphorus level fell from 9.2 +/- 0.6 to 2.8 +/- 0.3 mg/dl. Before therapy, the serum phosphorus level correlated positively with the serum glucose level, the effective plasma osmolality, and anion gaps, and correlated negatively with the serum chloride level. It is concluded that hyperphosphatemia is common in diabetic ketoacidosis before therapy. The increase in serum phosphorus is likely to be due to a transcellular shift. Potential factors responsible for the shift are serum glucose, through its osmotic effect, and the organic anions.
The New England Journal of Medicine | 1978
Pravit Cadnapaphornchai; Barbara F. Rosenberg; Saadi Taher; Eric H. Prosnitz; Franklin D. McDonald
MALAKOPLAKIA, described in 1902,1 is an unusual chronic inflammatory disease generally confined to the collecting system of the urinary tract. Renal parenchymal involvement is rare and was bilatera...
Journal of Critical Care | 1994
James A. Kruse; Pravit Cadnapaphornchai
Estimation and measurement of serum osmolality can be of value in the clinical management of certain forms of critical illness. Osmolality is a measure of the concentration of osmotically active particles, or solutes, in a solution. Only low-formula weight ions and uncharged molecules that are present in relatively high concentrations contribute significantly to serum osmolality. Serum osmolality can be easily estimated from the three major osmotic constituents of normal serum (sodium, urea, and glucose) by a simple formula. An understanding of serum osmolality, its laboratory measurement, its bedside estimation, and the concept of the osmole gap, is crucial in making a preliminary diagnosis of methanol and ethylene glycol intoxication, as well as a few other related compounds. There are important caveats to this use of the osmole gap, because under certain circumstances both false-positive and false-negative interpretations may occur. The osmole gap may also be helpful for confirming pseudohyponatremia, as a gauge for dosing mannitol and glycerol when used to treat intracranial hypertension, and as a prognostic indicator in circulatory shock.
The American Journal of the Medical Sciences | 1980
Pravit Cadnapaphornchai; Saadi Taher; Franklin D. McDonald
Thirty patients with drug associated acute nontraumatic rhabdomyolysis were evaluated. Acute renal failure, oliguric (ORF) in ten and nonoliguric (NORF) in another ten patients, was observed. The remaining ten patients did not develop renal failure (NRF). To identify factors that may have contributed to this clinical diversity, these three groups were compared. Data from 51 patients reported in the literature were also included in the analysis. The patients with ORF were slightly younger than patients with NORF, They had higher incidence of muscle swelling and higher serum potassium. ORF was more severe, lasted longer, and required more dialysis than NORF. The group of patients with renal failure had higher incidence of coma and more patients with very hight muscle enzyme elevation than NRF patients. Hypercalcemia, a unique complication of rhabdomyolysis, was reported in 22 patients. It was not seen in patients without renal failure. There were no differences in age, incidence of coma, muscle swelling, and muscle enzyme between those who did and those who did not develop hypercalcemia. Sixteen patients with nerve entrapment had higher incidence of coma and muscle swelling than the rest of the patients.
Annals of Emergency Medicine | 1981
Pravit Cadnapaphornchai; Saadi Taher; Dinyar B. Bhathena; Franklin D. McDonald
We report a case of ethylene glycol poisoning in a 54-year-old man found comatose on the street. No history was available. The diagnosis was based on the findings of a high anion gap metabolic acidosis, a high osmolal gap, and the presence of oxalate and hippurate crystals in the urine. The diagnosis was confirmed later by an ethylene glycol level of 775 mg/dl. This case illustrates how these parameters can be used in the emergency department for rapid diagnosis and management.
Prostaglandins | 1978
Pravit Cadnapaphornchai; Gary Aisenbrey; Keith M. McDonald; Thomas J. Burke; Robert W. Schrier
Acute elevation of ureteral pressure to 100 mm Hg in anesthetized dogs (n=7) resulted in an increase (P less than 0.005) in systemic blood pressure form 151 +/- 7 to 163 +/- 7 mm Hg, a transient (approximately 15 min) increase (P less than 0.05) in renal blood flow from 413 +/- 27 to 465 +/- 27 ml/min and a rise (P less than 0.05) in plasma renin activity from 6.0 +/- 1.6 to 10.3 +/- 2.1 ng/ml/hr. Pretreatment with a competitive inhibitor of angiotensin II, i.e. sar1gly8AII, abolished the hypertensive response to acute ureteral obstruction, and pretreatment with 2 mg/kg of either indomethacin (n=6) or meclofenamate (n=3), 15 min before obstruction, prevented the hyperemic response. These results suggest that acute ureteral obstruction leads to hypertension via activation of the renin-angiotensin system and hyperemia via a prostaglandin-initiated mechanism.
The American Journal of Medicine | 1974
Pravit Cadnapaphornchai; K.Chakko Kuruvila; Joseph H. Holmes; Robert W. Schrier
Abstract We are reporting a detailed analysis of our 5 year experience with 78 home hemodialysis patients whose mean age was 39 years. All but 4 of 46 patients who had hypertension during the course of their dialysis were controlled by fluid removal and antihypertensive medications. Only two of eight patients who had positive hepatitis B antigen had clinical evidence of hepatitis. Persistent ascites was found in eight patients; four of these patients responded to either transplantation or intensive hemodialysis. Peripheral neuropathy was progressive in four diabetic patients but remained stable in nine other patients with neuropathy. Roentgenographic evidence of bone disease was found in 67.1 per cent of patients, and 21 per cent of them had fractures. The cumulative survival for the 78 patients was 95.9, 87.6, 68.7 and 53.4 per cent at 0.5, 1, 2, and 3 years, respectively. The major causes of death were cardiovascular, infectious complications and voluntary termination of dialysis. This analysis of our experience in home dialysis has allowed prospective planning in an attempt to improve both the survival and quality of life of home hemodialysis patients. The need for intensive and continuous socioeconomic and psychologic evaluation is discussed.
PLOS ONE | 2015
Zeenat Yousuf Bhat; Pravit Cadnapaphornchai; Kevin Ginsburg; Milani Sivagnanam; Shamit Chopra; Corey Treadway; Ho Sheng Lin; George H. Yoo; Ammar Sukari; Mona D. Doshi
Acute kidney injury (AKI) is a well-known complication of cisplatin-based chemotherapy; however, its impact on long-term patient survival is unclear. We sought to determine the incidence and risk factors for development of cisplatin-associated AKI and its impact on long-term renal function and patient survival. We identified 233 patients who received 629 cycles of high-dose cisplatin (99±9mg/m2) for treatment of head and neck cancer between 2005 and 2011. These subjects were reviewed for development of AKI. Cisplatin nephrotoxicity (CN) was defined as persistent rise in serum creatinine, with a concomitant decline in serum magnesium and potassium, in absence of use of nephrotoxic agents and not reversed with hydration. All patients were hydrated per protocol and none had baseline glomerular filtration rate (GFR) via CKD-EPI<60mL/min/1.73m2. The patients were grouped based on development of AKI and were staged for levels of injury, per KDIGO-AKI definition. Renal function was assessed via serum creatinine and estimated glomerular filtration rate (eGFR) via CKD-EPI at baseline, 6- and 12-months. Patients with AKI were screened for the absence of nephrotoxic medication use and a temporal decline in serum potassium and magnesium levels. Logistic regression models were constructed to determine risk factors for cisplatin-associated AKI. Twelve-month renal function was compared among groups using ANOVA. Kaplan-Maier curves and Cox proportional hazard models were constructed to study its impact on patient survival. Of 233 patients, 158(68%) developed AKI; 77 (49%) developed stage I, 55 (35%) developed stage II, and 26 (16%) developed stage III AKI. Their serum potassium and magnesium levels correlated negatively with level of injury (p<0.05). African American race was a significant risk factor for cisplatin-associated AKI, OR 2.8 (95% CI 1.3 to 6.3) and 2.8 (95% CI 1.2 to 6.7) patients with stage III AKI had the lowest eGFR value at 12 months (p = 0.05) and long-term patient survival (HR 2.1; p<0.01) than patients with no or lower grades of AKI. Most common causes of death were recurrent cancer (44%) or secondary malignancy elsewhere (40%). Cisplatin-associated severe AKI occurs in 20% of the patients and has a negative impact on long-term renal function and patient survival. PEG tube placement may be protective and should be considered in high risk-patients.
The American Journal of Medicine | 1974
K.Chakko Kuruvila; Pravit Cadnapaphornchai; Georgia Leasor; Mordecai Popovtzer; Allen C. Alfrey; Robert W. Schrier
Abstract In an effort to better rehabilitate patients on home dialysis by shortening the duration of effective dialysis and thereby permitting evening hemodialysis, the simultaneous use of two hollow fiber artificial kidneys (HFAK) was evaluated. The clearances of urea, creatinine, uric acid, phosphate, iothalamate and cyanocobalamin were substantially higher than those obtained with any available single dialyzer. These clearances also were significantly enhanced by use of the single pass dialysate delivery system as compared to the recirculating single pass system. The clearances were comparable whether the blood flow through the two HFAK was in parallel or in series. Reuse of the HFAK was feasible, thus minimizing any economic disadvantage of the system. In eight patients, who have used the system at home for 9 to 12 hours per week for up to 6 months, weight, blood pressure, serum chemistries and motor nerve conduction have remained stable. This shorter dialysis with the double HFAK system allows for evening dialysis, thus freeing daytime hours for productive activity and nighttime for sleep.
Experimental Biology and Medicine | 1989
Pravit Cadnapaphornchai; Debra Kellner; Franklin D. McDonald
Abstract We have previously shown that diphenylhydantoin (DPH)-stimulated renin release is mediated by, or requires the presence of, the renal nerves. In the present study, we examined the effects of adrenergic blockers in DPH-stimulated renin release in five groups of anesthetized dogs. In vehicle-treated dogs, DPH at a dose of 0.18 mg/kg-min increased renin secretion rate (RSR) from 56 ± 14 to 269 ± 60 and returned to 84 ± 30 ng of angiotensin (ANG) I/hr-min (P < 0.01, analysis of variance). In metoprolol-treated dogs, DPH produced no significant changes in RSR (90 ± 28 to 144 ± 67 to 100 ± 51 ng of ANG I/hr-min). Likewise, in atenolol-treated dogs, RSR was 34 ± 10 before, 59 ± 15 during, and 23 ± 8 ng of ANG I/hr-min after the infusion of DPH. In contrast, after pretreatment with ICI 118,551 (a β 2 adrenoceptor antagonist), RSR was 37 ± 9 before, 151 ± 57 during, and 47 ± 12 ng of ANG I/hr-min after the infusion of DPH (P < 0.01). In phentolamine-treated dogs, RSR was 69 ± 20 before, 295 ± 53 during, and 95 ± 17 ng of ANG I/hr-min after the infusion of DPH (P < 0.01). Changes in renal blood flow, renal vascular resistance, and UNaV were in the same directions in all groups. These data suggest that DPH-stimulated renin release is mediated by β 1 adrenoceptors since both β 2 and α adrenoceptor antagonists have no effects on DPH-stimulated renin release.