Medical Student Clinical Pearl – January 2020

Carine Nzirorera

Faculty of Medicine
Dalhousie University
CC3
Class of 2021

Carine Nzirorera- ResearchGate

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual

Acute kidney injury (AKI) is defined as an abrupt decrease in kidney function and is classified based on changes in serum creatinine level, reduction of urine output, and need for renal replacement therapy ^[1]. The Kidney Disease: Improving Global Outcomes (KDIGO) is the most preferred definition and staging system. According to KDIGO guidelines AKI is define as an 1) increase in serum creatinine by ≥0.3 mg/dL (≥26.5 µmol/L) within 48 hours, or 2) an increase in serum creatinine ≥ 1.5 fold from baseline within 7 days, or 3) urine output <0.5 mL/kg/hour for 6 hours ^[2].

KDIGO staging criteria ^[2]

Stage 1 an increase of serum creatinine level of 1.5 to 1.9 times baseline, OR increase in serum creatinine by ≥0.3mg/dL (≥26.5 µmol/L) OR a urine output less than 0.5 mL/kg/hour for 6 to 12 hours.

Stage 2 an increase of serum creatinine level of 2 to 2.9 times baseline OR a urine output less than 0.5 mL/kg/hour for more than 12 hours.

Stage 3 an increase of serum creatinine level of greater than 3 times baseline OR increase in serum creatinine to ≥4.0 mg/dL (≥353.6 µmol/L), OR a urine output less than 0.3 mL/kg/hour for ≥24 hours OR anuria output ≥12 hours OR initiation of renal replacement therapy such as dialysis.

Case Presentation

69y male with a history of kidney stones had experienced 1 week of hematuria, 1 month of bilateral flank pain and unintentional 20 lbs weight loss over 2 months. Patient was scheduled for a CT scan of his urinary tract and was urgently sent to emergency department after his creatinine levels were found to be severely elevated (2300 µmol/L).

Patient had a 20 year history of kidney stones and previous abdominal CT scans showed small stones in both kidneys =/< 2mm. Patient was afebrile, had no dysuria or increased frequency but complained of difficulty initiating urination and noticed a reduction of the stream even when his bladder felt full. Patient noted no vomiting, diarrhea or decrease in fluid and food intake. Patient had a positive family history of bladder cancer and was a smoker for 30+ years.

Etiology

Causes of acute kidney injury are organized based on located of the insult (Table 1) ^[1]. Causes related to decrease in renal perfusion are classified as prerenal injury. Decrease renal perfusion is seen in sepsis due to decreased arterial pressure from systemic vasodilation; intravascular volume depletion from vomiting, diarrhea or overuse of diuretics can also reduce circulation to the kidneys [1]. Lastly drugs like nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitor can lower intraglomerular pressure causing reduced glomerular filtration rate. NSAIDs and calcineurin inhibitors constrict afferent (or preglomerular) arterioles while ACE inhibitors and angiotensin receptor blockers dilate efferent (or postglomerular) arterioles ^[3].

Direct renal damage to glomeruli, tubules, interstitium or vasculature are classified as Renal injury. Nephritides can be caused by infection (viral, bacterial, and fungal), medication (antibiotics, antivirals, protein pump inhibitors) toxins (ethylene glycol, aminoglycoside, rhabdomyolysis) or are secondary to conditions like hypertension, prolonged hypotension, lupus, diabetes mellitus and vasculitis.

Impaired drainage of urine distal to the kidneys due to obstruction of the urinary tract is classified as Postrenal cause of acute kidney injury.  Common causes of obstruction are kidney stones, injury, prostate, cervical or bladder cancer.

Previously 70% of community acquired cases of acute kidney injury are classified as prerenal causes ^[4], a more recent study found 55% of community acquired acute kidney injury were renal disease, 35% pre-renal disease and 10% were postrenal ^[5].

Clinical Presentation, History and Physical Exam

Clinical presentation of acute kidney injury varies with severity and varies with prerenal, renal and postrenal causes (Table 2). Patients with mild to moderate acute kidney injury are usually asymptomatic and identifiable by laboratory testing. Severe cases would present with vomiting, confusion, fatigue, anorexia, nausea, weight gain or edema ^[6]. Decline in mental status, asterixis or neurologic symptoms can be indicative of uremic encephalopathy, anemia or bleeding caused by uremic platelet dysfunction ^[1].

History and physical exam should determine cause of the kidney injury. Screening questions should be used to determine renal perfusion, any potential source of renal injury and any symptoms suggestive of obstructive uropathy (Table 2). Decreased renal perfusion can be assumed from a history of gastrointestinal illness, poor oral intake, use of diuretics, NSAIDs or ACE inhibitors ^[1,7]. Past medical history of diabetes mellitus, cardiac or liver disease can also indicate reduced renal perfusion ^[1,7]. Source of renal injury can be screen by assessing current medication for recent antibiotics, antiviral and protein pump inhibitors use, inquiring about past medical history of systemic illnesses such as lupus, viral, bacterial, or fungal infection or symptoms of infection such as rash, arthralgias, fatigue, and hematuria ^[1,7]. Postrenal cause can be determined from a history of gross hematuria, difficulty urinating, urgency or hesitancy to urinate or a history of kidney stones or bladder, prostate or cervical cancer ^[1,7].

Case continued

Blood work

• CBC: elevated leukocytes (13.5) decreased erythrocytes (3.32), decreased hemoglobin (97), decreased Hematocrit (0.304) normal MCV
• INR (1.2) APTT (44.3)
• Liver function test were normal
• Creatinine (2300)
• Venous blood gas: decreased pH (7.17), decreased bicarbonate (13), pCO2 (36) and lactate (1.9 )
• Electrolytes: elevated potassium (7.9), decreased sodium (131), decreased chloride (93), elevated glucose (10.7)

Figure 1. ECG of patient showing Sinus Rhythm and peaked T waves in V2, V3, and V4, an early manifestation of hyperkalemia. Other manifestations (not demonstrated here) include prolonged PR segment, loss of P wave, bizarre QRS complexes and sine wave.

PoCUS Imaging

Figure 2. Ultrasound imaging showing moderate hydronephrosis, areas of anechoic fluid indicated by red arrows.

CT Imaging

Figure 3. A) Pelvic CT showing bladder with diffuse wall thickening with a posterior globular neoplasm. B) Pelvic CT showing bladder with calculi within the neoplasm. C) Abdominal CT showing moderate bilateral hydronephrosis.

Diagnosis

It was determined that the cause of the acute kidney injury was diffuse thickening of the bladder wall causing obstruction of the ureterovesical junctions (Figure 3A and B). This resulted in bilateral moderate hydronephrosis (Figure 2 and 3C). Additionally, previous CBC reports showed the patient had chronic anemia likely from an underlying chronic kidney disease. This affected EPO production and resulted in decreased erythrocytes production from bone marrow.  With reduce erythrocytes, hemoglobin and hematocrit levels were also decreased. The acute kidney injury resulted in elevated creatinine level, leading to hyperkalemia and metabolic acidosis.

Management

Patient was admitted and fluid resuscitated. To correct his hyperkalemia patient was given 5 to 10 units of regular insulin and dextrose 50% intravenously to shift potassium out of circulation and into the cells. Calcium gluconate (10 mL of 10% solution infused over 5 mins) was given to reduce risk of arrhythmias.

To treat his bilateral hydronephrosis patient was sent to interventional radiology for placement of percutaneous nephrostomy tube. Follow up surgery will be needed to clear the ureters and biopsy of the bladder will be needed to determine treatment for the growth.  Depending on the remaining kidney function after treatment of the acute kidney injury the patient may require dialysis.

References

1. Rahman, Mahboob, Fariha Shad, and Michael C. Smith. “Acute kidney injury: a guide to diagnosis and management.” American family physician 86.7 (2012): 631-639.
2. KDIGO Clinical Practice Guideline for Acute Kidney Injury, Kidney Int Suppl. 2012;2(Suppl 1):8
3. Erdbruegger Uta, Okausa Mark. “Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults”. Uptodate (2019)
4. Kaufman J, Dhakal M, Patel B, Hamburger R. Community-acquired acute renal failure. American Journal of Kidney Disease 2 (1991): 191–198.
5. Obialo CI, Okonofua EC, Tayade AS, Riley LJ. Epidemiology of de novo acute renal failure in hospitalized African Americans: Comparing community‐acquired vs hospital‐acquired disease. Archives of Internal Medicine 160.9 (2000): 1309– 13.
6. Meyer TW, Hostetter TH. Uremia. New England Journal of Medicine 357.13 (2007): 1316–1325.
7. Mesropian, Paul Der, et al. “Community‐acquired acute kidney injury: A challenge and opportunity for primary care in kidney health.” Nephrology 21.9 (2016): 729-735.