Postrenal azotemia

Last updated: February 23, 2023

Postrenal azotemia

D&M1

D&M1

Gas exchange in the lungs, blood and tissues
Diffusion-limited and perfusion-limited gas exchange
Compliance of lungs and chest wall
Anatomy of the lungs and tracheobronchial tree
Blood pressure, blood flow, and resistance
Carbon dioxide transport in blood
Anatomy clinical correlates: Pleura and lungs
Regulation of pulmonary blood flow
Compliance of blood vessels
Resistance to blood flow
Zones of pulmonary blood flow
Airflow, pressure, and resistance
Changes in pressure-volume loops
Laminar flow and Reynolds number
Anatomy of the heart
Cardiac conduction system
ECG rate and rhythm
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Sympathetic nervous system
Measuring cardiac output (Fick principle)
Cardiac work
Coronary circulation
Ventilation
Ventilation-perfusion ratios and V/Q mismatch
Clinical Skills: Mechanical ventilation - conventional ventilators
Reading a chest X-ray
Cardiac cycle
Cardiac preload
Cardiac afterload
Cardiac contractility
Body fluid compartments
Movement of water between body compartments
Hydration
The role of the kidney in acid-base balance
Hyponatremia
Hyponatremia: Clinical
Hypernatremia
Hypernatremia: Clinical
Electrolyte disturbances: Pathology review
Kidney histology
Hyperkalemia
Hyperkalemia: Clinical
Hypokalemia
Hypokalemia: Clinical
Hypercalcemia
Hypocalcemia
Phosphate, calcium and magnesium homeostasis
Hypomagnesemia
Hypermagnesemia
Respiratory acidosis
Metabolic acidosis
Metabolic and respiratory acidosis: Clinical
Plasma anion gap
Metabolic alkalosis
Respiratory alkalosis
Acute kidney injury: Clinical
Prerenal azotemia
Renal azotemia
Renal failure: Pathology review
Postrenal azotemia
Renal clearance
Renal system anatomy and physiology
Body temperature regulation (thermoregulation)
Blood histology
Blood components
Erythropoietin
Innate immune system
Introduction to the immune system
Cell-mediated immunity of CD4 cells
T-cell development
T-cell activation
B- and T-cell memory
B-cell development
Cell-mediated immunity of natural killer and CD8 cells
Aplastic anemia
Heparin-induced thrombocytopenia
Coagulation (secondary hemostasis)
Role of Vitamin K in coagulation
Coagulation disorders: Pathology review
Disseminated intravascular coagulation
Liver anatomy and physiology
Liver histology
Pancreatic secretion
Gastrointestinal system anatomy and physiology
Esophageal motility
Gastric motility
Jaundice: Pathology review
Delirium
Dementia and delirium: Clinical
Traumatic brain injury: Pathology review
Traumatic brain injury: Clinical
Concussion and traumatic brain injury
Brain herniation
Blood brain barrier
Anatomy of the cranial base
Anatomy of the cerebral cortex
Introduction to the cranial nerves
Cranial nerve pathways
Anatomy of the olfactory (CN I) and optic (CN II) nerves
Central nervous system histology
Peripheral nervous system histology
Nervous system anatomy and physiology
Neuron action potential
Parasympathetic nervous system
Hypophosphatemia
Hyperphosphatemia
Selective permeability of the cell membrane
Gluconeogenesis
Lung volumes and capacities

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 with postrenal AKI, there’s some obstruction to the outflow from the kidneys.

Reduced flow can be a result of something compressing the ureter like intra-abdominal tumors, or compressing the urethra further down, like from benign prostatic hyperplasia—a noncancerous growth of the prostate gland, both of which sort of pinch the ureter or urethra shut.

Also though it could be some blockage inside, like kidney stones getting stuck in the ureter or urethra, which actually plug it up. Now, if only one ureter’s obstructed, called unilateral obstruction, and the other kidney’s working fine, then renal function’s usually preserved. If, say, both ureters are obstructed, called bilateral obstruction, or the urethra gets blocked, then we’ve got a recipe for postrenal AKI.

Whatever the obstruction is, it ultimately causes this buildup of urine and pressure that backs up into the kidney; all the way to the millions of tiny renal tubules.

Key Takeaways

Postrenal azotemia is a condition characterized by an excessive level of nitrogen-containing waste products in the bloodstream (azotemia) due to obstruction of the urinary tract. Postrenal azotemia can be caused by congenital abnormalities such as vesicoureteral reflux, blockage of the ureters by kidney stones, pregnancy, compression of the ureters by cancer, prostatic hyperplasia, or blockage of the urethra by kidney or bladder stones. Postrenal azotemia can lead to kidney failure if left untreated. Treatment typically involves medical or surgical interventions to remove the obstruction.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Acute kidney injury" The Lancet (2019)
  6. "Management of severe hyperkalemia" Critical Care Medicine (2008)
  7. "Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group" Critical Care (2004)