Intrinsic acute kidney injury (glomerular causes): Clinical sciences

Intrinsic acute kidney injury or AKI refers to a sudden decline in kidney function that results in electrolyte imbalances, extracellular dysregulation, and the accumulation of nitrogenous waste, such as ammonia and uric acid. The underlying cause of intrinsic AKI can be glomerular, which involves damage to the glomerulus; and non-glomerular, which affects renal components like tubules or the interstitium.

If your patient presents with chief concerns suggesting AKI, first, perform an ABCDE assessment to determine if they’re unstable or stable. If unstable, stabilize their airway, breathing, and circulation. Next, obtain IV access, which might include dialysis access, and put your patient on continuous vital sign monitoring and cardiac telemetry. Finally, if you identify hyperkalemia, metabolic acidosis, volume overload, or symptomatic uremia, start emergent hemodialysis!

Now, let’s go back and take a look at stable patients. First, obtain a focused history and physical exam, which usually reveals nonspecific signs and symptoms. For example, history might reveal reduced urine output, bloody urine, or systemic symptoms, like fatigue, malaise, and fever. Additionally, patients might report taking nephrotoxic medications or having chronic conditions, like systemic lupus erythematosus or malignancy.

Similarly, the physical exam is nonspecific and might reveal blood pressure abnormalities, rash, or periorbital and peripheral edema. In this case, suspect intrinsic AKI, so be sure to order a basic metabolic panel and urinalysis with microscopy, assess the patient’s urine output over time, and check renal ultrasound!

In all types of AKI, labs will reveal a rise in serum creatinine of 0.3 milligrams per deciliter or more over 48 hours; a rise of serum creatinine 1.5 times the baseline or more in the last 7 days, or urine output less than 0.5 milliliters per kilogram per hour for six hours. However, with intrinsic AKI, the BUN-to-Cr ratio will be less than 20 to 1, and urine sodium will be greater than 20 milliequivalents per liter.

Next, calculate the fractional excretion of sodium, or FENa for short, to check the percentage of sodium filtered by the kidneys into the urine. Divide the product of urinary sodium and serum creatinine by the product of urinary creatinine and serum sodium and multiply the dividend by 100. In intrinsic AKI, kidneys fail to reabsorb the sodium from filtered urine, meaning more sodium gets excreted, so the FENa will be greater than 2 percent.

Now, here’s a clinical pearl! In contrast to intrinsic AKI, in prerenal AKI, the kidneys filter less sodium to maintain intravascular volume. In other words, the FENa will be below 1%. Remember, FENa is not reliable in oliguric individuals with chronic kidney disease because this condition is associated with an impaired ability to concentrate urine and varying baseline plasma sodium levels. In other words, FENa will not adequately reflect the changes in acute kidney injury. Similarly, FENa is not reliable in oliguric patients who are taking diuretics because these medications promote sodium excretion and can give falsely high FENa values.

Additionally, urinalysis and microscopy often reveal RBC casts, WBC casts, or tubular epithelial casts. Finally, if the renal ultrasound shows normal kidneys and parenchyma with no hydronephrosis, you can diagnose intrinsic AKI, which can occur due to glomerular and non-glomerular causes.

Now, let’s focus on glomerular causes, which include proliferative glomerulonephritis and non-proliferative glomerulonephropathy! Patients with proliferative glomerulonephritis typically report fever, joint pain, and frankly bloody or dark-colored urine. Next, the exam will reveal facial or peripheral edema and hypertension, while the urinalysis with microscopy will reveal hematuria, dysmorphic RBCs, and RBC casts. With these findings, diagnose proliferative glomerulonephritis, more specifically, a nephritic pattern of glomerular injury.

Here’s a clinical pearl! Proliferative glomerulonephritis typically presents with a nephritic pattern of injury. However, in severe cases, patients might present with nephrotic syndrome, characterized by massive proteinuria and hypoalbuminemia.

Now, to assess the specific type, order additional labs, including CBC, complement C3 and C4, and cryoglobulins. Also, test for autoantibodies, including c-ANCA-, p-ANCA-, anti-glomerular basement membrane-, antinuclear-, and anti-double stranded DNA antibodies. Finally, order a renal biopsy and assess underlying causes.

First, let’s focus on IgA nephropathy, also called Berger disease, which is associated with recurrent episodes of hematuria. Patients might also report a recent upper respiratory infection or a history of liver- or celiac disease. If renal biopsy reveals mesangial deposits of IgA along the basement membrane, diagnose IgA nephropathy.

Treatment focuses on supportive care for AKI. If there’s hypovolemia, start intravenous hydration, and if there’s volume overload, stimulate diuresis with diuretics. In severe cases, you can begin dialysis to manage potassium, urea, and acid base balance until the kidneys recover. Also, correct any electrolyte disturbances and be sure to control blood pressure. Finally, don’t forget glucocorticoids for refractory cases.

Next up is anti-glomerular basement membrane disease, formerly called Goodpasture syndrome, which is associated with the deposition of anti-GBM antibodies along the glomerular basement membrane. As a result, the immune system impairs glomerular filtration, causing symptoms like reduced urine output.

Remember, these antibodies can also deposit along the alveolar membrane and cause dyspnea, cough, and even massive hemoptysis. If labs reveal positive anti-GBM antibodies, and the renal biopsy shows linear IgG deposition along the glomerular basement membrane, diagnose anti-GBM disease.

Treatment includes supportive care, glucocorticoids, and immunosuppressants like cyclophosphamide. Finally, if there’s acute hemoptysis or hematuria, consider plasmapheresis to remove circulating antibodies.