ACUTE KIDNEY INJURY (AKI)
Acute kidney injury should be considered in any patient has-
*Increase in the serum creatinine concentration from baseline (>26 mmol/L within 48 hours)
*Percentage serum creatinine increase >50%
*Oliguria of less than 0.5 mL/kg per hour for more than six hours (or <500mL/day for an adult). Remember, normal UOP is approximately 1mL/kg/hour = 1500mL/day for a 60kg adult.
Diagnostic Approach- Things you should consider for all patients. Kidney injury in the hospital is often tied into another problem (infection, heart failure, medications).
1. Get a good history and check the vital signs, including orthostatics!
*decreased or no urine output, flank pain, edema, hypertension, or discolored urine? Hesistancy, frequency?
*weakness and easy fatiguability (from anemia), anorexia, vomiting, diarrhea, mental status changes or seizures, and edema?
*fever, cough, dysuria? Bleeding (i.e. melena, blood per rectum)?
*new/changed doses in medications?
2. Check a urinalysis, including sediment (can be done in histopathology).
3. Check BUN and creatinine. If serum and urine electrolytes can also be checked you should calculated the FENa which is a measure of how much sodium the kidney is excreting.
4. Check abdominal ultrasound to rule out obstruction and assess the size and echotexture of the kidneys.
5. Monitor urine output (UOP) closely. Strongly consider catheterization, especially in setting of enlarged prostate or full bladder on exam.
6. You should try and determine if this is chronic or acute. Does the patient have medical problems that pre-dispose to renal disease (i.e. HIV, diabetes, HTN)? Renal ultrasound shows small kidneys in most forms of CKD.
| Etiologies | U/A, sediment, Indices | |
Prerenal* | Hypovolemia (bleeding, diarrhea) Systemic vasodilation (infection) Decreased cardiac output (heart failure) Renal vasoconstriction (ACEI, NSAIDS, cirrhosis) Large vessel (thrombosis, embolism, dissection) | Bland (no cells) FEna<1% BUN/Cr>20 (in mg/dL) |
| Intrinsic | Acute Tubular Necrosis (ATN)* Ischemia: prolonged pre-renal Toxins: drugs (aminoglycosides), pigments (rhabdo), protein Contrast induced | Pigmented granular “muddy brown” casts (~75% of cases) FENa>2% (except in pigment and contrast types) |
| Acute Interstital Nephritis Allerigc: sulfa, b-lactams, NSAIDs, traditional meds Infection: pyelonephritis Infiltrative: sarcoid, lymphoma, leukemia | WBCs, WBC casts, +/- RBCs +eosinophils in abx induced (~90%) +lymphs in NSAIDs | |
| Renovascular (small vessel) HUS/TTP, DIC, pre-eclampsia, HTN crisis*, endocarditis | +/- RBCs | |
| Glomerulonephritis* | Dysmorphic RBCs & RBC casts | |
| Postrenal | Bladder neck: BPH, prostate CA, schisto* Ureteral: malignancy, LAD, nephrolithiasis Tubular: precipitation of crystals | Bland US will show dilation of the renal pelvis |
* Most common causes AKI in our setting.
Treatment Options-
1. Treat the underlying disorder. Consider fluid boluses if you think the patient is dehydrated. Aim to increase the UOP to at least 100mL/hour. Listen to their lungs frequently, make sure they are not getting fluid overloaded. Monitor blood pressure closely.
2. If patient is bleeding, make sure you check PT/INR; consider blood transfusion.
3. Monitor for signs of uremia (i.e. mental status changes, vomiting). Also monitor electrolytes, as these can be deranged in renal failure.
4. Stop all nephrotoxic agents, such as NSAIDs or aminoglycosides.
5. Redose meds based on GFR.
Indications for urgent dialysis:
Acid-base disturbance (academia)
Electrolyte disorder (usually hyperkalemia)
Intoxication (methanol, ethylene glycol, lithium, salicylates)
Overload of volume (pulmonary edema)
Uremia (pericarditis, encephalopathy, severe bleeding)
| Signs and Sxs of Uremia | |
| General | Nausea, anorexia, malaise, fetor uremicus, metallic taste, pruritis, uremic frost |
| Neurologic | Encephalopathy (change in mental status, decreased memory and attention), seizures, neuropathy |
| Cardiovascular | Pericarditis, HTN, volume overload, CHF, cardiomyopathy, hyperlipidemia, accelerated atherosclerosis |
| Hematologic | Anemia, bleeding (due to platelet dysfunction) |
| Metabolic | Hyperkalemia, hyperphosphatemia, acidosis, hypocalcemia, secondary hyperparathyroidism, osteodystrophy |
CHRONIC KIDNEY DISEASE (CKD)
Definition:
* >= 3 months of reduced GFR and or kidney damage (abnormal pathology, blood/urine markers, or imaging)
* Most common etiologies include diabetes, HTN, HIV, glomerulonephritis, polycystic kidney disease, drug-induced, multiple myeloma, progression of AKI (like severe obstruction)
| Stages of CKD | ||
| Stage | GFR | Goals |
| 1 | >90 * | Dx/rx of underlying condition and comorbidities; slow progression; cardiovascular risk reduction |
| 2 (mild) | 60-89 | Estimate progression |
| 3 (moderate) | 30-59 | Evaluate and treat complications |
| 4 (severe) | 15-29 | Begin preparation for renal replacement therapy (dialysis) |
| 5 (kidney failure) | <15 or on dialysis | Dialysis if uremic |
* with proteinuria
Complications of CKD:
- Anemia – due to decreased production of erythropoietin (+ other factors)
- Hyperkalemia – due to decreased potassium excretion
- Hyperphosphatemia / Hypocalcemia – due to decreased phosphate excretion and binding of phosphate to calcium
- Acidemia – due to decreased H+ excretion
- Low Vit D 1,25 / Secondary Hyperparathyroidism / renal osteodystrophy – decreased activation of Vit D causes hyperparathyroidism and painful breakdown of bones
- Edema – due to decreased sodium excretion and hyperaldosteronism
- Uremia - due to decreased excretion of urea and other toxins
Treatment:
1. control risk factors for progression of CKD (ex: tight glycemic control if diabetic)
2. BP control, goal <130/80, start with an ACEI as first line medication (nephroprotective)
3. monitor for and treat complications: iron +/- erythropoietin to maintain hgb 7-10, low potassium diet / potassium binders, phosphate binders, give Vit D1,25, lasix for edema, dialysis or renal transplant for uremia
4. Avoid Nephrotoxins
Estimating the Glomerular Filtration Rate (GFR) based on the Cockroft & Gault equation:
Creatinine Clearance (ml/min) = 1.23 x ( (140-age) x weight (kg) ) / Creatinine (umol/l) )
For women = 1.04 x ( (140-age) x weight (kg) ) / Creatinine (umol/l) )
CASE
A 60 yo M with a h/o HTN (not on medications) comes to clinic with a complaint of lower extremity edema that has been slowly getting worse over the course of the last several months. On ROS there is no fever, chest pain, shortness of breath, palpitations or decreased urine output. Past medical history is otherwise unremarkable. Social history is significant for a history of smoking 4-5 cigarettes/day for the last 20 years. Family history is significant for a mother with DMII. Exam reveals 1+ pitting edema to the mid shin. The patient is overweight, mildly pale and there are no signs of IDS. The CV exam is normal. The patient’s blood pressure is 140/90. He weighs 80kg.
1) What is your impression? CKD
2) What investigations will you request? Creatinine, UA. RBG
The creatinine returns as 250umol/liter. The UA showed 2+ proteinuria. The RBG is 12.
1) What is your impression now, be specific. DMII, HTN, CKD
2) Are you surprised that the urine output is still normal? UOP usually normal in CKD
3) How will you estimate the patient’s GFR? Cockroft Gault Equation using creatinine . GFR = 25!
4) What stage of CKD is this patient? Stage 4. Review concept of staging and how we stage based on GFR to determine complications expected and treatment.
5) What complications of CKD will you look for?Review complications of CKD as above.
6) What treatments will you initiate? As above, 4 considerations.
You are following the patient in clinic but the patient is admitted to the ICU for pneumonia and sepsis. While in the ICU he received gentamycin as well as fluids. After several days of treatment his symptoms and vital signs have improved however you now note that his urine output has gradually been decreasing to the point where he is producing <30cc/hour. Currently his BP is stable at 120/70, pulse is 70, he is not orthostatic. There is no edema by examination. The bladder is not enlarged and the kidney is not enlarged by examination.
1) What is your impression now? AKI (on CKD)
2) What investigations do you want to order? BUN/Cr, electrolytes, ECG, Renal US, UA, Examination of Urine Sediment
3) What treatment will you initiate? Stop aminoglycosides, fluid challenge.
You stop the patient’s gent and start him instead on ciprofloxacin. The patient’s creatinine is 600umol/L. Potassium is 4.3. The UA is negative for WBC, bacteria, LE or nitrates. You take a sample of urine to Dr. Kahima for centrifuge and microsocopy and it shows muddy brown casts. Renal ultrasound reveals no hydronephrosis. The kidneys are small with poor differentiation of the renal cortex and medulla.
1) What is your impression now? Be precise. ATN
2) What are the things that cause AKI? Review classification of prerenal, renal and postrenal AKI and subgroups.
3) What is the most likely cause of AKI in this patient? Aminoglycosides, hypotension
4) What physical exam findings should you be following closely on this patient? Mental status, asterixis, listen for rub.
5) What other investigations would you want to follow closely on this patient? BUN/Cr, electrolytes, ECG
You continue conservative management for a presumptive diagnosis of ATN. The patient remains oliguric and over the next week he begins complaining of nausea and SOB. His exam is now significant for a blood pressure of 175/95. He has crackles in his bilateral lobes. He has a pericardial rub and 1+ LEE. He seems confused. You are still waiting for blood work to return however his EKG from today reveals peaked T waves.
1) What should you do while you await the results of his bloodwork? Review treatment of hyperkalemia
2) What are the indications for urgent dialysis? As above with pneumonic.
You presumptively treat the patient for hyperkalemia with insulin, glucose, kayexalate. In the meantime you begin to arrange for the patient to be transferred to another hospital so that he may be started on dialysis.
