THE DIURNAL VARIATIONS OF THE DIASTATIC CONTENT OF NORMAL URINE

1923 ◽  
Vol 1 (4) ◽  
pp. 91-94 ◽  
Author(s):  
Gordon Cameron
1970 ◽  
Vol 24 (01/02) ◽  
pp. 026-032 ◽  
Author(s):  
N. A Marsh

SummaryMolecular exclusion chromatography was performed on samples of urine from normal and aminonucleoside nephrotic rats. Normal urine contained 2 peaks of urokinase activity, one having a molecular weight of 22,000 and the other around 200,000. Nephrotic urine contained three peaks of activity with MW’s 126,000, 60,000 and 30,000. Plasma activator determined from euglobulin precipitate had a MW. in excess of 200,000. The results indicate that in the normal animal, plasma plasminogen activator does not escape into the urine in substantial quantities but under the conditions of extreme proteinuria there may be some loss through the kidney. The alteration in urokinase output in nephrotic animals indicates a greatly disordered renal fibrinolytic enzyme system.The findings of this study largely support the hypothesis that plasma plasminogen activator of renal origin and urinary plasminogen activator (urokinase) are different molecular species.


1983 ◽  
Vol 104 (2_Supplb) ◽  
pp. S177-S187
Author(s):  
J. Odink ◽  
H. Sandman ◽  
A.J. Speek ◽  
W.H.P. Schreurs

2016 ◽  
Vol 94 (suppl_5) ◽  
pp. 418-418
Author(s):  
F. Rosa ◽  
J. S. Osorio ◽  
J. Lohakare ◽  
M. Moridi ◽  
A. Ferrari ◽  
...  

Author(s):  
Jaimin R. Patel

Bladder outlet obstruction (BOO) produces compression or resistance upon the bladder outflow channel at any location from the bladder neck to urethral meatus. It may be induced by specific functional and anatomic causes. Functional obstruction may be caused by detrusor-sphincter dyssynergia (DSD) and anatomic obstruction most commonly from benign prostatic enlargement (BPH) or urethral stricture. Obstructive symptoms include hesitancy, sensation of incomplete bladder emptying, diminished urinary stream. The combination of PVR, urinary flow measures, and symptom appraisal has been generally accepted as the initial screening and evaluation paradigm for BOO. In, Ayurveda, BOO is similar to Mutraghata means obstruction in the urine flow. Uttarbasti is the prime treatment of Mutraghata. Present case is diagnosed as a functional bladder outlet obstruction (BOO) on the basis of symptoms, normal reports of USG and ascending urethrogram and diminished flow of urine in Uroflowmetry. Total 7 Uttarbasti with 50ml Sahcharadi Tailam was given along with Rasayana and Mutraghatahara medicine. Patient has complete relief in his obstructive urine complains and has normal urine flow without taking Tab. AFDURA after 7 years. And also improvement appear in Uroflowmetry.


2011 ◽  
Vol 45 (16) ◽  
pp. 6784-6792 ◽  
Author(s):  
Akihiro Fushimi ◽  
Rota Wagai ◽  
Masao Uchida ◽  
Shuichi Hasegawa ◽  
Katsuyuki Takahashi ◽  
...  

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
T. M. Skipina ◽  
S. Macbeth ◽  
E. L. Cummer ◽  
O. L. Wells ◽  
S. Kalathoor

Abstract Introduction Acute encephalopathy, while a common presentation in the emergency department, is typically caused by a variety of metabolic, vascular, infectious, structural, or psychiatric etiologies. Among metabolic causes, hyperammonemia is relatively common and typically occurs in the setting of cirrhosis or liver dysfunction. However, noncirrhotic hyperammonemia is a rare occurrence and poses unique challenges for clinicians. Case presentation Here we report a rare case of a 50-year-old Caucasian female with history of bladder cancer status post chemotherapy, radical cystectomy, and ileocecal diversion who presented to the emergency department with severe altered mental status, combativeness, and a 3-day history of decreased urine output. Her laboratory tests were notable for hyperammonemia up to 289 μmol/L, hypokalemia, and hyperchloremic nonanion gap metabolic acidosis; her liver function tests were normal. Urine cultures were positive for Enterococcus faecium. Computed tomography imaging showed an intact ileoceal urinary diversion with chronic ileolithiasis. Upon administration of appropriate antibiotics, lactulose, and potassium citrate, she experienced rapid resolution of her encephalopathy and a significant reduction in hyperammonemia. Her hyperchloremic metabolic acidosis persisted, but her hypokalemia had resolved. Conclusion This case is an example of one of the unique consequences of urinary diversions. Urothelial tissue is typically impermeable to urinary solutes. However, when bowel segments are used, abnormal absorption of solutes occurs, including exchange of urinary chloride for serum bicarbonate, leading to a persistent hyperchloremic nonanion gap metabolic acidosis. In addition, overproduction of ammonia from urea-producing organisms can lead to abnormal absorption into the blood and subsequent oversaturation of hepatic metabolic capacity with consequent hyperammonemic encephalopathy. Although this is a rare case, prompt identification and treatment of these metabolic abnormalities is critical to prevent severe central nervous system complications such as altered mental status, coma, and even death in patients with urinary diversions.


1916 ◽  
Vol 28 (1) ◽  
pp. 237-240
Author(s):  
C.Ferdinand Nelson ◽  
W.E. Burns

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