Kidney Anatomy, Function and Physiology

Kidney Anatomy and Function

• Kidneys are located in the retroperitoneal area between T12 and L3.
• Right kidney sits slightly lower than the left due to the liver.
• Renal colic refers to kidney pain that can radiate to the toes.
• Kidney functions include excretion of waste products, blood purification, and urine production.
• Urine contains phosphates, urea, and creatinine.
• The kidneys regulate blood pressure through the renin hormone.
• Erythropoietin, a hormone needed for red blood cell production, is normally produced by the kidneys.
• Renin increases blood pressure, and this can be blocked by ARBs (renin-angiotensin blockers).
• Blood urea and creatinine are waste products; creatinine results from protein breakdown, while blood urea comes from muscle breakdown.
• Kidneys filter approximately 1.50 liters of blood in 24 hours; a complete cycle of blood filtration occurs in less than an hour.
• Nephrons within the kidneys perform blood filtration; a kidney typically has multiple nephrons.
• The glomerulus is the primary filtering unit within the nephron.
• After purification, urine flows from the renal pelvis to the bladder via the ureters.
• The bladder has a capacity of about 750ml.
• Micturition (urination) is controlled by the center of the pons, involving both voluntary and involuntary muscles.

Acute Kidney Injury (AKI)

• AKI involves the accumulation of waste products due to issues like dehydration, diarrhea, or vomiting, leading to increased BUN and creatinine levels and low urine output.
• Prerenal AKI: Causes include severe dehydration, heart failure, and low cardiac output, which result in low blood pressure and reduced blood flow to the kidneys.
• Intrarenal AKI: Direct damage to the kidneys caused by nephrotoxic medications (e.g., mycin antibiotics, metformin, IV contrast).
• Metformin should be stopped hours before CT scans, and kidney labs should be checked.
• Post-renal AKI: Obstruction of urine flow.
• Conditions such as drug use and prolonged immobility can lead to myoglobinuria and subsequently AKI.
• Acute kidney injury is potentially reversible with proper management, unlike chronic kidney disease, which is irreversible.
• The kidneys excrete potassium and reabsorb bicarbonate to buffer acid.
• Hypovolemia can lead to AKI due to decreased kidney perfusion.

Clinical Manifestations and Phases of AKI

• AKI can be reversed if addressed promptly where antibiotics require renal labs to be checked because the kidneys filter them.
• Diuretic phase: Indicates recovery.
• Oliguric phase: Characterized by urine output less than 400ml per day or 20ml per hour, lasting 10-14 days, with possible dark urine, casts, RBCs, and WBCs present.
• Oliguric phase symptoms include edema, fluid overload, heart failure, crackles, labored breathing, low oxygen saturation, hypertension, low heart rate, and JVD. Fluid retention during this phase can lead to pulmonary edema.
• Metabolic acidosis often presents with Kussmaul respirations due to the impaired ability of the kidneys to excrete acid. Sodium balance: Hyponatremia can lead to cerebral changes and altered consciousness.
• Potassium excess: Hyperkalemia is often asymptomatic.
• Neurologic disorders: Fatigue, difficulty concentrating, seizures, stupor, and coma can occur.
• Other signs include decreased urinary output, neurological changes, tiredness, itchiness, and hyperkalemia.
• Diuretic phase: Characterized by daily urine output of 1-3 liters, leading to potential dehydration, hyponatremia, and hypokalemia.

Treatment and Management of AKI

• Fluid replacement: IV fluids are administered for blood loss, but be cautious of causing edema.
• Regular vancomycin level checks is important, adjusting dosage for kidney function.
• Lab monitoring: Check sodium, potassium, blood urea, and creatinine levels
• Kidney stones: Ultrasound can be used for detection.
• Biopsy: Confirms the diagnosis and assesses the degree of kidney damage.
• In emergency situations, CT scans should be performed without IV contrast to avoid further kidney damage.
• Managing patients with massive blood loss-induced AKI involves fluid administration.
• For oliguria, loop diuretics such as Lasix and mannitol can be used cautiously.
• In cases of fluid overload, diuretics should be used carefully.
• Hyperkalemia treatment: Administering 10 units of IV insulin along with dextrose to shift potassium into cells.
• Metabolic acidosis treatment: Administer sodium bicarbonate.
• Calcium carbonate can be administered.
• Sodium polystyrene sulfonate (Kayexalate) is used to eliminate potassium via feces.
• It's important to confirm bowel sounds before administering Kayexalate to avoid bowel necrosis.
• Emergency dialysis: May be necessary for patients with severe symptoms like pulmonary edema and fluid overload, especially when they do not respond to conventional treatments like sodium bicarbonate, fluids, and Lasix.
• Renal Replacement Therapy (RRT): Can be continuous in the intensive care unit for patients with unstable blood pressure.
• Nutrition therapy: Includes restricting sodium and potassium intake while avoiding protein restriction.
• Monitoring: Vital signs, fluid intake and output, signs of fluid overload, mental status and consciousness, heart rhythm, daily weight, and electrolytes.
• Replace significant fluid losses and avoid nephrotoxic medications.

Critical Scenarios

• For a patient with hypovolemic shock and AKI, dialysis would not be the first option.
• Instead of standard 4-hour dialysis, continuous renal replacement dialysis (CRRT) is preferred and continue for 24 hours in the ICU

Concise kidney anatomy review covering location, function, and urine production. The kidneys regulate blood pressure, produce erythropoietin, and filter approximately 1.50 liters of blood in 24 hours. Nephrons within the kidneys perform blood filtration.