Prerenal azotemia

Last updated: February 23, 2023

Prerenal azotemia

PBL MS2 S1 Exam 3

PBL MS2 S1 Exam 3

Alcohol-associated liver disease
Liver anatomy and physiology
Benign liver tumors
Non-alcoholic fatty liver disease
Anatomy of the abdominal viscera: Liver, biliary ducts and gallbladder
Hepatic encephalopathy
Wilson disease
Ischemia
Cirrhosis
Cirrhosis: Pathology review
Jaundice
Portal hypertension
Hemochromatosis
Autoimmune hepatitis
Alpha 1-antitrypsin deficiency
Primary sclerosing cholangitis
Neonatal hepatitis
Hepatocellular carcinoma
Reye syndrome
Viral hepatitis
Primary biliary cholangitis
Hepatocellular adenoma
Blood histology
Blood components
Erythropoietin
Blood groups and transfusions
Platelet plug formation (primary hemostasis)
Role of Vitamin K in coagulation
Coagulation (secondary hemostasis)
Clot retraction and fibrinolysis
Iron deficiency anemia
Beta-thalassemia
Alpha-thalassemia
Sideroblastic anemia
Anemia of chronic disease
Lead poisoning
Hemolytic disease of the newborn
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Autoimmune hemolytic anemia
Pyruvate kinase deficiency
Paroxysmal nocturnal hemoglobinuria
Sickle cell disease (NORD)
Hereditary spherocytosis
Aplastic anemia
Fanconi anemia
Megaloblastic anemia
Folate (Vitamin B9) deficiency
Vitamin B12 deficiency
Diamond-Blackfan anemia
Hemophilia
Vitamin K deficiency
Bernard-Soulier syndrome
Glanzmann's thrombasthenia
Hemolytic-uremic syndrome
Immune thrombocytopenia
Thrombotic thrombocytopenic purpura
Antithrombin III deficiency
Factor V Leiden
Protein C deficiency
Protein S deficiency
Antiphospholipid syndrome
ACE inhibitors, ARBs and direct renin inhibitors
Osmotic diuretics
Carbonic anhydrase inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Potassium sparing diuretics
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal and urinary tract masses: Pathology review
Posterior urethral valves
Hypospadias and epispadias
Vesicoureteral reflux
Bladder exstrophy
Urinary incontinence
Neurogenic bladder
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Renal agenesis
Horseshoe kidney
Potter sequence
Hyperphosphatemia
Hypophosphatemia
Hypernatremia
Hyponatremia
Hypermagnesemia
Hypomagnesemia
Hyperkalemia
Hypokalemia
Hypercalcemia
Hypocalcemia
Renal tubular acidosis
Minimal change disease
Diabetic nephropathy
Focal segmental glomerulosclerosis (NORD)
Amyloidosis
Membranous nephropathy
Lupus nephritis
Membranoproliferative glomerulonephritis
Poststreptococcal glomerulonephritis
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Alport syndrome
Kidney stones
Hydronephrosis
Acute pyelonephritis
Chronic pyelonephritis
Prerenal azotemia
Renal azotemia
Acute tubular necrosis
Postrenal azotemia
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Angiomyolipoma
Nephroblastoma (Wilms tumor)
WAGR syndrome
Beckwith-Wiedemann syndrome
Physiologic pH and buffers
Buffering and Henderson-Hasselbalch equation
The role of the kidney in acid-base balance
Acid-base map and compensatory mechanisms
Respiratory acidosis
Metabolic acidosis
Plasma anion gap
Respiratory alkalosis
Metabolic alkalosis
Osmoregulation
Sodium homeostasis
Antidiuretic hormone
Kidney countercurrent multiplication
Free water clearance
Potassium homeostasis
Phosphate, calcium and magnesium homeostasis
Renin-angiotensin-aldosterone system
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
Tubular reabsorption and secretion
Tubular secretion of PAH
Tubular reabsorption of glucose
Urea recycling
Tubular reabsorption and secretion of weak acids and bases
Renal clearance
Glomerular filtration
TF/Px ratio and TF/Pinulin
Measuring renal plasma flow and renal blood flow
Regulation of renal blood flow
Hydration
Body fluid compartments
Movement of water between body compartments
Renal system anatomy and physiology
Drug administration and dosing regimens
Ureter, bladder and urethra histology
Sexually transmitted infections: Clinical
Vulvovaginitis: Clinical
Sexually transmitted infections: Warts and ulcers: Pathology review
Haemophilus ducreyi (Chancroid)
Pelvic inflammatory disease
Chlamydia trachomatis
Premature rupture of membranes: Clinical
Neisseria gonorrhoeae
Endometritis
Gardnerella vaginalis (Bacterial vaginosis)
Cervical cancer
Cervical cancer: Pathology review
Viral hepatitis: Pathology review
Cell wall synthesis inhibitors: Penicillins
Cell wall synthesis inhibitors: Cephalosporins
Miscellaneous cell wall synthesis inhibitors
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Beta blockers
Adrenergic receptors
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Cardiac contractility
Frank-Starling relationship
Class I antiarrhythmics: Sodium channel blockers
Class III antiarrhythmics: Potassium channel blockers
Class II antiarrhythmics: Beta blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Long QT syndrome and Torsade de pointes
Calcium channel blockers
Heart failure: Clinical
Positive inotropic medications
Acute kidney injury: Clinical
Kidney stones: Clinical
Multiple endocrine neoplasia: Pathology review
Endocrine system anatomy and physiology
Multiple endocrine neoplasia
Pancreatic secretion
von Hippel-Lindau disease
Pancreatic neuroendocrine neoplasms
Pancreas histology
Pancreatitis: Pathology review
Pancreatic cancer
Acute pancreatitis
Hypopituitarism
Pancreatitis: Clinical
Prolactinoma
Zollinger-Ellison syndrome
Lung cancer
Cell signaling pathways
MEN syndromes: Clinical
Chronic pancreatitis
Adrenal masses: Pathology review
Pituitary apoplexy
Pituitary gland histology
Pituitary adenomas and pituitary hyperfunction: Clinical
Pituitary tumors: Pathology review
Pituitary adenoma
Hypopituitarism: Clinical
Precocious puberty
Polycystic ovary syndrome
Oxytocin and prolactin
Premature ovarian failure
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Menopause
Cushing syndrome: Clinical
Hunger and satiety
Hypothyroidism: Pathology review
Constitutional growth delay
Adrenal masses and tumors: Clinical
Hyperthyroidism: Clinical
Hypothyroidism
Sheehan syndrome
Adrenal gland histology
Primary adrenal insufficiency
Congenital adrenal hyperplasia
Adrenal cortical carcinoma
Adrenal insufficiency: Pathology review
Adrenal hormone synthesis inhibitors
Congenital adrenal hyperplasia: Clinical
Adrenal insufficiency: Clinical
Synthesis of adrenocortical hormones
Waterhouse-Friderichsen syndrome
Cushing syndrome
Cushing syndrome and Cushing disease: Pathology review
Testosterone
Diabetes mellitus: Clinical
Diabetes insipidus
Diabetes mellitus: Pathology review
Diabetes mellitus
Diabetes insipidus and SIADH: Pathology review
Managing diabetes during the holidays: Information for patients and families
Hypernatremia: Clinical
Acromegaly
Streptococcus pneumoniae
Atherosclerosis and arteriosclerosis: Pathology review
Gigantism
Leg ulcers: Clinical
Chronic kidney disease: Clinical
Preeclampsia & eclampsia
Progestins and antiprogestins
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Spina bifida
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Dilated cardiomyopathy
Abnormal labor: Clinical
Contraception: Clinical
B-cell development
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Gestational trophoblastic disease: Clinical
Routine prenatal care: Clinical
Abdominal pain: Clinical
Pediatric vomiting: Clinical
Ovarian cysts, cancer, and other adnexal masses: Clinical
Antepartum hemorrhage: Clinical
Abnormal uterine bleeding: Clinical
Perinatal infections: Clinical
Hypertensive disorders of pregnancy: Clinical
Complications during pregnancy: Pathology review
Ectopic pregnancy
Pregnancy

Flashcards

Prerenal azotemia

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Questions

USMLE® Step 1 style questions USMLE

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 A 40-year-old man presents to the emergency department with difficulty breathing over the past two days. His past medical history is significant for chronic liver disease secondary to chronic alcohol use disorder. His temperature is 36.6°C (97.8° F), pulse is 80/min, respirations are 21/min, and blood pressure is 125/80 mm Hg. Physical examination shows abdominal distention with shifting dullness. Serum creatinine concentration is 1.5 mg/dL (reference range: 0.6-1.2 mg/dL), and serum urea nitrogen concentration is 20 mg/dL (7-18 mg/dL). The patient is started on furosemide, and his condition quickly improves. Three days later, repeated laboratory studies show the following:

 Laboratory value  Result  Reference range 
 Serum  
 Sodium  132 mEq/L  136-146 mEq/L 
 Potassium  4.2 mEq/L  3.5-5 mEq/L 
 Chloride  95 mEq/L  95-105 mEq/L 
 Creatinine  1.9 mg/dL  0.6-1.2 mg/dL 
 Albumin  3.2 g/dL  3.5-5.5 g/dL 
 BUN/Cr  > 20:1  10:1-20:1 
 Urine  
 Erythrocytes  0/hpf  0-4/hpf 
 Leukocytes  2/hpf  0-5/hpf 
 Fractional excretion of sodium (FENa <1%  1-2% 
 Urine osmolality  600 mOsm/kg  50-1,400 mOsm/kg 
 Sediment  None  None 


Which of the following is the most likely explanation for these laboratory findings?

Transcript

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Content Reviewers

Acute kidney injury, or AKI, is when the kidney isn’t functioning at 100% and that decrease in function develops relatively quickly, typically over a few days. Actually, AKI used to be known as acute renal failure, or ARF, but AKI is a broader term that also includes subtle decreases in kidney function.

AKI can essentially be split into three types, prerenal AKI meaning the cause of kidney injury’s coming before the kidneys, postrenal AKI—meaning after the kidneys, or intrarenal AKI—meaning within the kidneys.

Now the kidney’s job is to regulate what’s in the blood, so they might remove waste, or make sure electrolyte levels are steady, or regulate the overall amount of water, and even make hormones - the kidneys do a lot of stuff!

Blood gets into the kidney through the renal artery, into tiny clumps of arterioles called glomeruli where it’s initially filtered, with the filtrate, the stuff filtered out, moving into the renal tubule.

Sometimes fluid or electrolytes can move back from the filtrate into the blood - called reabsorption, and sometimes more fluid or electrolytes can move from the blood to the fitrate - called secretion.

Along with fluid and electrolytes, though, waste-containing compounds are also filtered, like urea and creatinine, although some urea is actually reabsorbed back into the blood, whereas only a little bit of creatinine is reabsorbed. In fact, in the blood, the normal ratio of blood urea nitrogen, or BUN, to creatinine is between 5 and 20 to 1—meaning the blood carries 5 to 20 molecules of urea for every one molecule of creatinine, and this is a pretty good diagnostic for looking at kidney function!

Ultimately the filtrate is turned into urine and is excreted from the kidney through the ureter, into the bladder, and peed away. Meanwhile, the filtered blood drains into the renal vein.

Alright so prerenal kidney injury is due to a decreased blood flow into the kidneys.

So if you’ve got your body fluid, with fluid in circulating in the plasma as well as all the other intracellular and extracellular fluid. So a decreased blood flow could be due to an absolute loss of body fluid, where fluid actually leaves the body.

This could be due to major hemorrhage or blood loss, vomiting, diarrhea, or with severe burns where body fluid evaporates quickly without the protective skin. Decreased blood flow could also be due to a relative loss of fluid, where total body fluid stays the same, how can that happen though?

Well one example of this is distributive shock, which is where fluid moves from the blood vessels into the tissues, which keeps the total body fluid volume the same but you have a relative decrease in blood volume.

Key Takeaways

Prerenal azotemia is a form of azotemia in which the kidneys fail to adequately filter waste products from the blood, due to reduced renal perfusion. This can be caused by dehydration, excessive blood loss, heart failure, or any condition that decreases blood flow to the kidneys. Treatment of prerenal azotemia focuses on addressing the underlying cause, such as increasing fluid intake or treating the underlying condition.