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azurekangaroo935Lv1

28 Sep 2019

If a substance appears in the renal artery but not in the renal vein:

It must be reabsorbed by the kidney

Its clearance is equal to GFR

It has the âfiltration onlyâ mechanism

Its plasma clearance is equal to RPF

Its urinary concentration must be higher than its plasma concentrationd

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ibaddr555Lv1

28 Dec 2021

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28 Sep 2019

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Related questions

Please help me answer the questions below in reference to the reading below as well:

Infusion of ketone bodies to ammonium chloride-loaded acidotic dogs was found to induce significant reduction in urin#ary excretion of ammonia. This effect could not be attributed to urinary pH variations. (1) Total ammonia production by the left kidney was measured in 25 animals infused during 90 min with the sodium salt of D,L-Î²-hydroxybutyric acid adjusted to pH 6.0 or 4.2. Ketonemia averaged 4.5 mM/liter. (2) . In all experiments the ammonia content of both urine and renal venous blood fell markedly so that ammoniogenesis was depressed by 60% or more within 60 min after the onset of infusion. (3). Administration of equimolar quantities of sodium acetoacetate adjusted to pH 6.0 resulted in a 50% decrease in renal ammonia production. (4) Infusion of ketone bodies adjusted to pH 6.0 is usually accompanied by a small increase in extracellular bicarbonate (3.7 mM/liter). However infusion of D,L-sodium lactate or sodium bicarbonate in amounts sufficient to induce a similar rise in plasma bicarbonate resulted in only a slight decrement in ammonia production (15%). The continuous infusion of 5% mannitol alone during 90-150 min failed to influence renal ammoniogenesis. (5) Infusion of pure sodium-free Î²-hydroxybutyric acid prepared by ion exchange (pH 2.2) resulted in a 50% decrease in renal ammoniogenesis in spite of the fact that both urinary pH and plasma bicarbonate fell significantly. (6) During all experiments where ketones were infused, the renal extraction of glutamine became negligible as the renal glutamine arteriovenous difference was abolished. Renal hemodynamics did not vary significantly. Infusion of Î²-hydroxybutyrate into the left renal artery resulted in a rapid decrease in ammoniogenesis by the perfused kidney. (7) The present study indicates that ketone bodies exert their inhibitory influence within the renal tubular cell. Since their effect is independent of urinary or systemic acid-base changes, it is suggested that they depress renal ammoniogenesis by preventing the transformation of glutamine and glutamate into Î±-ketoglutarate in the mitochondria of the renal tubular cell. (8)

QUESTION 1: Why do you think that infusion of pure sodium-free Î²-hydroxybutyric acid prepared resulted in a 50% decrease in renal ammoniogenesis in spite of the fact that both urinary pH and plasma bicarbonate fell significantly.

QUESTION 2:

Why do you think that infusion of Î²-hydroxybutyrate into the left renal artery resulted in a rapid decrease in ammoniogenesis by the perfused kidney.

beigeimpala281

Question 1: Why do you think that the adding of sodium acetoacetate resulted in a 50% decrease in renal ammonia production?

Question 2: Explain how ketone bodies depress renal ammoniogenesis by preventing the transformation of glutamine and glutamate into Î±-ketoglutarate in the mitochondria of the renal tubular cell.

Excerpt:

Infusion of ketone bodies to ammonium chloride-loaded acidotic dogs was found to induce significant reduction in urinary excretion of ammonia. This effect could not be attributed to urinary pH variations. Total ammonia production by the left kidney was measured in 25 animals infused during 90 min with the sodium salt of D,L-Î²-hydroxybutyric acid adjusted to pH 6.0 or 4.2. Ketonemia averaged 4.5 mM/liter. In all experiments the ammonia content of both urine and renal venous blood fell markedly so that ammoniogenesis was depressed by 60% or more within 60 min after the onset of infusion. Administration of equimolar quantities of sodium acetoacetate adjusted to pH 6.0 resulted in a 50% decrease in renal ammonia production. Infusion of ketone bodies adjusted to pH 6.0 is usually accompanied by a small increase in extracellular bicarbonate (3.7 mM/liter). However infusion of D,L-sodium lactate or sodium bicarbonate in amounts sufficient to induce a similar rise in plasma bicarbonate resulted in only a slight decrement in ammonia production (15%). The continuous infusion of 5% mannitol alone during 90-150 min failed to influence renal ammoniogenesis.

Infusion of pure sodium-free Î²-hydroxybutyric acid prepared by ion exchange (pH 2.2) resulted in a 50% decrease in renal ammoniogenesis in spite of the fact that both urinary pH and plasma bicarbonate fell significantly. During all experiments where ketones were infused, the renal extraction of glutamine became negligible as the renal glutamine arteriovenous difference was abolished. Renal hemodynamics did not vary significantly. Infusion of Î²-hydroxybutyrate into the left renal artery resulted in a rapid decrease in ammoniogenesis by the perfused kidney. The present study indicates that ketone bodies exert their inhibitory influence within the renal tubular cell. Since their effect is independent of urinary or systemic acid-base changes, it is suggested that they depress renal ammoniogenesis by preventing the transformation of glutamine and glutamate into Î±-ketoglutarate in the mitochondria of the renal tubular cell.

orangeguinea-pig426

Case-3: Patient History

P.W. is 23 years old. He was the victim of a hit-and-run auto-pedestrian accident and suffered multiple abrasions, a concussion, and a deep laceration of his left thigh. He was discovered approximately 2 hours after the incident and is now in the emergency department. P.W.âs vital signs and hematocrit suggest that he has had a blood loss of about 2500 ml. A urinary catheter is inserted to monitor urine output, and fluid resuscitation is initiated while his wounds are cleaned and sutured. The urine output is averaging 15 ml/hr, with a high urine osmolality and low urine sodium.

What type of renal failure is P.W. likely developing? (select all that apply)

Intrarenal acute renal failure

Prerenal acute renal failure

Postrenal acute renal failure

Chronic renal failure

Based on your answer for the previous question, what is the best therapy for preventing this from occurring? (select all that apply)

Adequate extracellular volume replacement with blood or isotonic fluids to ensure adequate circulating blood volume and perfusion pressure to the kidney is essential.

Antibiotic therapy should be administered immediately.

Restriction of fluid intake to prevent increase in circulating blood volume and perfusion pressure to the kidney is essential.

Dialysis should be initiated immediately.

In addition to urine output, what laboratory data should be monitored to assess changes in P.W.âs renal function? (select all that apply)

Serum BUN, creatinine, and potassium should be monitored. A decrease indicates decreased renal function.