mediates increased release of aldosterone.

is not expressed in the kidney.

has a more pronounced vasoconstriction on the afferent rather than the efferent arteriole.

is the receptor for angiotensin I.

protects against ischemia-reperfusion injury by intrarenal dilation.

ET-1 release reduces renal blood flow.

Stimulation of endothelin-1 (ET-1) decreases sodium excretion.

ET-1 release stimulates aldosterone secretion.

ET-1 release is inhibited by nitric oxide.

Endothelin is the most potent vasoconstrictor yet identified.

Angiotensin II

Norepinephrine

Carbon monoxide

Endothelin

Atrial natriuretic peptide

Hemoxygenase-2 (HO-2) is a constitutive enzyme.

HO-1 is an inducible enzyme.

HO-1 expression helps to maintain renal medullary blood flow. e. HO-1 produces CO through the catabolism of heme.

Increased carbon monoxide (CO) increases ischemiareperfusion injury in the kidney.

Reduced erythropoiesis and anemia are common in chronic renal disease.

The kidney makes most of the erythropoietin in the body.

There are erythropoietin receptors in many organs of the body.

During chronic inflammation, erythropoiesis is decreased.

Erythropoiesis is inhibited by low circulating oxygen tension.

Normal compensation for hyponatremia is decreased antidiuretic hormone (ADH) secretion and thirst suppression.

If asymptomatic hyponatremia does not improve within 24 hours, intravenous hypertonic saline should be started.

By definition, hypernatremia is always associated with elevated total body sodium content.

Abnormal elevation of serum lipids can lead to a false, elevated measurement of serum sodium.

In therapy for symptomatic hyponatremia, the goal should be a normal serum sodium value of 135 mEq/L within 48 hours.

may be treated with lithium or demeclocycline.

is associated with high total body sodium.

is always seen in patients with hypervolemic.

is triggered by low circulating volume.

is associated with decreased aquaporin expression in the kidney.

Too rapid correction can lead to a cerebral demyelination syndrome.

Intranasal desmopressin is a useful adjuvant therapy.

Fluid overload as a result of hypertonic saline infusion should be treated with a loop diuretic such as furosemide.

Aggressive therapy should be discontinued when the serum sodium concentration is raised 10% or symptoms subside.

For acute severe hyponatremia with symptoms, a typical infusion rate of hypertonic saline would be 1 mL/kg/hr.

results in impairment of maximum concentrating ability of the kidney due to loss of the medullary osmotic gradient.

is associated with hypervolemid.

is associated with mutations of the genes producing aldosterone.

is associated with inappropriately concentrated urine.

may be classified as nephrogenic or urogenic.

Acidosis drives potassium out of the cell into the circulation.

Upper limit for safe intravenous potassium infusion is 40 mEq/hr.

Potassium is primarily an intracellular ion.

Angiotensin-converting enzyme (ACE) inhibitors may be a cause of hypokalemia.

High-sodium load in the distal tubule promotes potassium excretion.

Nebulized albuterol can reduce serum potassium by promoting an intracellular shift of potassium.

Intravenous calcium does not lower serum potassium but is given to protect the heart from the effects of hyperkalemia.

Hyperkalemia can cause peaked T waves on the electrocardiogram (ECG).

Hemolysis of the blood sample may falsely elevate the measured potassium.

All patients with a serum potassium value greater than 5.5╯mEq/L require immediate therapy.

Ammonia (NH4) is the most important buffer in the blood.

Normal pH in the blood is 7.56 to 7.60.

Immediate response to an acid load is through buffers in the blood.

Normal body metabolism produces less than 1000 mmol of acid per day.

All acids produced by metabolism can be excreted by the lungs.

Ammonium ion (NH+ 4) is produced from glutamine, primarily by proximal tubular cells.

Lungs can excrete volatile acid, but the kidneys must excrete fixed acid.

Most bicarbonate is reabsorbed in the distal collecting tubule.

Chronic respiratory acidosis should lead to increased H+ in the kidney.

Carbonic anhydrase catalyzes the production of H+ and HCO− 3 from H2O and CO2.

pure respiratory acidosis.

a blood buffer system that is not working.

a mixed acid-base disturbance.

acidemia.

pure metabolic acidosis.

direct bicarbonate loss from the kidney would lead to metabolic acidosis and a normal anion gap.

appropriate respiratory compensation for a metabolic acidosis is decreased respiration with an increased PCO2.

It is not possible to have both a respiratory and metabolic acidosis at the same time.

lactic acidosis usually presents as a nonanion gap metabolic acidosis.

increasing the blood HCO− 3 level increases the anion gap.