Prerenal azotemia

Last updated: February 23, 2023

Prerenal azotemia

Watch later

Watch later

Parathyroid hormone
Calcitonin
Vitamin D
Insulin
Glucagon
Diabetes mellitus
Diabetes mellitus: Pathology review
Pancreatic neuroendocrine neoplasms
Hyperparathyroidism
Hypoparathyroidism
Parathyroid disorders and calcium imbalance: Pathology review
Insulins
Hypoglycemics: Insulin secretagogues
Miscellaneous hypoglycemics
Osteoporosis medications
Hypertrophic cardiomyopathy
Pigmentation skin disorders: Pathology review
Albinism
Thymus histology
Glomerular filtration
Measuring renal plasma flow and renal blood flow
Thyroglossal duct cyst
Bowel obstruction
Platelet plug formation (primary hemostasis)
Anatomy of the abdominal viscera: Kidneys, ureters and suprarenal glands
Anatomy of the perineum
Thiazide and thiazide-like diuretics
Vaginal and vulvar disorders: Pathology review
Alpha-thalassemia
Spleen histology
Fallopian tube and uterus histology
Mammary gland histology
Ovary histology
Brucella
Oral cancer
Oxygen binding capacity and oxygen content
Obstructive lung diseases: Pathology review
Ehrlichia and Anaplasma
Myeloproliferative disorders: Pathology review
Nervous system anatomy and physiology
Hyperkalemia
Dementia: Pathology review
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy clinical correlates: Heart
Anatomy clinical correlates: Mediastinum
Infectious endocarditis: Clinical sciences
Infective endocarditis: Clinical
Endocarditis
Endocarditis: Pathology review
Development of the respiratory system
Adenovirus
Anatomy of the arm
Perinatal infections: Clinical
Dyslipidemias: Pathology review
Acyanotic congenital heart defects: Pathology review
Blood pressure, blood flow, and resistance
ECG basics
Development of the cardiovascular system
Fetal circulation
Calcium channel blockers
Anatomy of the eye
Introduction to the cranial nerves
Cranial nerve pathways
Anatomy of the olfactory (CN I) and optic (CN II) nerves
Anatomy of the oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves
Anatomy of the trigeminal nerve (CN V)
Anatomy of the facial nerve (CN VII)
Anatomy of the vestibulocochlear nerve (CN VIII)
Anatomy of the glossopharyngeal nerve (CN IX)
Anatomy of the vagus nerve (CN X)
Anatomy of the spinal accessory (CN XI) and hypoglossal (CN XII) nerves
Anatomy clinical correlates: Facial (CN VII) and vestibulocochlear (CN VIII) nerves
Anatomy clinical correlates: Glossopharyngeal (CN IX), vagus (X), spinal accessory (CN XI) and hypoglossal (CN XII) nerves
Anatomy clinical correlates: Oculomotor (CN III), trochlear (CN IV) and abducens (CN VI) nerves
Anatomy clinical correlates: Olfactory (CN I) and optic (CN II) nerves
Anatomy clinical correlates: Trigeminal nerve (CN V)
Actinomyces israelii
Clostridium botulinum (Botulism)
Clostridium tetani (Tetanus)
Haemophilus influenzae
Listeria monocytogenes
Mycobacterium tuberculosis (Tuberculosis)
Neisseria meningitidis
Staphylococcus aureus
Staphylococcus epidermidis
Streptococcus agalactiae (Group B Strep)
Streptococcus pneumoniae
Central nervous system histology
Peripheral nervous system histology
Eye and ear histology
Coxsackievirus
Cytomegalovirus
Eastern and Western equine encephalitis virus
Epstein-Barr virus (Infectious mononucleosis)
Herpes simplex virus
JC virus (Progressive multifocal leukoencephalopathy)
Lymphocytic choriomeningitis virus
Measles virus
Mumps virus
Poliovirus
Rabies virus
Varicella zoster virus
West Nile virus
Acute disseminated encephalomyelitis
Central pontine myelinolysis
Multiple sclerosis
Transverse myelitis
Charcot-Marie-Tooth disease
Guillain-Barre syndrome
Adult brain tumors
Neurofibromatosis
Pediatric brain tumors
Pituitary adenoma
Sympathomimetics: Direct agonists
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
Cardiac muscle histology
Mesothelioma
Nasal polyps
Nasopharyngeal carcinoma
Pancoast tumor
Superior vena cava syndrome
Cystic fibrosis: Pathology review
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Pneumonia: Pathology review
Tuberculosis: Pathology review
Lung cancer and mesothelioma: Pathology review
Nasal, oral and pharyngeal diseases: Pathology review
Restrictive lung diseases: Pathology review
Apnea, hypoventilation and pulmonary hypertension: Pathology review
Deep vein thrombosis and pulmonary embolism: Pathology review
Respiratory distress syndrome: Pathology review
Adrenergic antagonists: Presynaptic
Adrenergic receptors
Cholinergic receptors
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympatholytics: Alpha-2 agonists
Introduction to the immune system
Gallbladder disorders: Pathology review
Anatomy of the thyroid and parathyroid glands
Acute coronary syndrome: Clinical sciences
Approach to chest pain: Clinical sciences
Approach to dyspnea: Clinical sciences
Approach to hypertension: Clinical sciences
Coronary artery disease: Clinical sciences
Diabetes mellitus (Type 1): Clinical sciences
Diabetes mellitus (Type 2): Clinical sciences
Dyslipidemia: Clinical sciences
Essential hypertension: Clinical sciences
Tobacco use: Clinical sciences
Ketone body metabolism
Kidney histology
Ureter, bladder and urethra histology
Bladder exstrophy
Horseshoe kidney
Hydronephrosis
Hypospadias and epispadias
Potter sequence
Renal agenesis
Alport syndrome
Goodpasture syndrome
IgA nephropathy (NORD)
Lupus nephritis
Poststreptococcal glomerulonephritis
Rapidly progressive glomerulonephritis
Amyloidosis
Diabetic nephropathy
Focal segmental glomerulosclerosis (NORD)
Membranoproliferative glomerulonephritis
Membranous nephropathy
Minimal change disease
Acute tubular necrosis
Renal papillary necrosis
Acute pyelonephritis
Chronic pyelonephritis
Lower urinary tract infection
Postrenal azotemia
Prerenal azotemia
Renal azotemia
Chronic kidney disease
Kidney stones
Renal tubular acidosis
Angiomyolipoma
Medullary cystic kidney disease
Medullary sponge kidney
Multicystic dysplastic kidney
Polycystic kidney disease
Beckwith-Wiedemann syndrome
Nephroblastoma (Wilms tumor)
Non-urothelial bladder cancers
Renal cell carcinoma
Transitional cell carcinoma
WAGR syndrome
Neurogenic bladder
Posterior urethral valves
Urinary incontinence
Vesicoureteral reflux
Renal artery stenosis
Renal cortical necrosis
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Hypercalcemia
Hypermagnesemia
Hypernatremia
Hyperphosphatemia
Hypocalcemia
Hypokalemia
Hypomagnesemia
Hyponatremia
Hypophosphatemia
Congenital renal disorders: Pathology review
Nephritic syndromes: Pathology review
Nephrotic syndromes: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal failure: Pathology review
Renal tubular acidosis: Pathology review
Renal tubular defects: Pathology review
Renal and urinary tract masses: Pathology review
Urinary incontinence: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Appendicitis
Abdominal hernias
Inguinal hernias: Clinical sciences
Femoral hernias: Clinical sciences
Umbilical hernias: Clinical sciences
Ventral and incisional hernias: Clinical sciences
Inguinal hernia
Femoral hernia
Acute pancreatitis: Clinical sciences
Cholecystitis: Clinical sciences
Peptic ulcer disease: Clinical sciences
Anticoagulants: Warfarin
Factor V Leiden

Transcript

Watch video only

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.