Oct 18, 2019
In this podcast, Dr. Carl Dean, a Nephrologist with Kidney Specialists of Minnesota, presented at Ridgeview Medical Center's Live Friday CME Series on September 27th, 2019. At this event, Dr. Dean provided information on acute kidney injury (AKI)- its frequency, management, and treatment modalities available for AKI.
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Nephrons are the functional unit of the kidneys. The nephrons have specialized capillary beds that have low partial pressures of oxygen which make kidneys susceptible to AKI.
The afferent/efferent capillary bed have a unique ability to constrict and dilate to maintain GFR during times of physiologic stress, this is called autoregulation.
The thickness of the renal cortex (or essentially where all the glomeruli are located) is important for detecting or estimating the chronicity of kidney disease. A thick cortex tells us that you have decreased renal function.
The proximal tubule is the workhorse of the nephron where the electrolytes, proteins and glucose are reabsorbed.
Podocytes are specialized epithelial cells that surround the capillary within the glomeruli assisting with the filtration system of the kidney. A strong electronegative charge. A classic disruption of this system leads to nephritic syndrome.
The kidney gets about 20% of blood flow from the heart.
Prostaglandins and Angiotensin 2 maintain GFR by driving constriction and dilation of the afferent and efferent capillary beds.
NSAIDS (diminish the ability to generate prostaglandins through arachidonic acid pathway), ARBs and ACE inhibitors inhibit -- Angiotensin 2 which generates constriction on the afferent and efferent cap beds (preferential on efferent).
Patients susceptible to AKI generally have preexisting chronic kidney disease.
We detect AKI through creatinine and urine output.
Factors that affect creatinine function include: age, gender, lean muscle mass, drugs (bacterium, cimetidine, tyrosine kinase inhibitors), ethnicity, diet.
NGAL, KIM-1 and IL-18 are true markers of structural injury to the kidney. They can be found in the serum as well as urine. NGAL and KIM-1 tend to go up rather fast with AKI in comparison to say creatinine. NGAL (neutrophil gelatinase-associated lipocalin) is one of the earliest and most robustly induced proteins in the kidney after ischemic or nephrotoxic AKI in animal models and KIM-1 (kidney injury molecule-1) is a type 1 transmembrane protein, with immunoglobulin and mucin domain, whose expression is markedly up-regulated in the proximal tubule in the post-ischemic rat kidney.
Pre-renal causes of CHF, hypovolemia, V/D, MI, PE, antihypertensives, anaphylaxis, cirrhosis, sepsis, hemorrhage, etc. Essentially: "The kidneys are not getting enough blood flow".
Post-renal causes include: obstruction can occur anywhere from renal tubule to the urethra. Generally, bilateral etiology to cause AKI.
1st step in evaluation for AKI is comparing present creatinine with previous and how rapidly the creatinine is rising.
Next, how is the patient feeling? Med review, screen of oral intake, loss, infection, etc. Recent procedures.
Labs to consider: UA, CBC, US, protein/CR ratio, CBC for TTP and micro-angiopathy. Additional testing include: Renal U/S, PTH, and anemia may give clues to the duration of decreased renal function/
Active Urine Sediment - concerning for acute glomerulonephritis, hematuria and proteinuria, hematuria, only <10% of hematuria is glomerular, >80% is bladder, prostate or urethra disease. Quantify the proteinuria, screening for glomerular disease and its severity. <1 g: significant glomerular disease unlikely, 1-3g: glomerular disease is likely. >3g: glomerular disease is present.
Hyaline casts (Tamm Horsfall) made in Loop of Henle tell us that there is low flow through the tubules. (Generally a pre-renal issue). Granular cast or muddy brown cast which is pathognomonic for ATN which is generally the diagnosis. RBC cast is generally concerning for acute glomerulonephritis may want to consider a nephron consult.
Renal U/S is generally recommended for every new AKI. This evaluate for size, hydronephrosis, 2 kidneys, cortical thickness.
Management of AKI is managing electrolytes and acidosis. Volume expansion. Trial of vasopressors, dialysis. No benefit to diuretics. Adjusting appropriate drug dosages for patient with AKI.
Furosemide stress test can be implemented as diagnostic test to determine the severity of the AKI in volume resus oliguria patient.
AKI in the hospital are likely something we did iatrogenic meds, CT contrast, hemodynamics, obstruction, sepsis, volume depletion.
Acute Interstitial Nephritis: Triad of rash, AKI and peripheral eosinophilia very rare (<10%). Need a high clinical suspicion. Although any drug can potentially cause DI-AIN, antibiotics, NSAIDS, and PPOIs are the most frequent offenders. Timing can be weeks to months until AKI develops. Renal biopsy confirms the diagnosis. Removal of offending drug sometimes use steroids.
Sepsis in AKI not well understood but thought 2nd to...
Macrovascular and microvascular dysfunction: Damage from inflammatory cytokines and leukocyte infiltration. Micro thrombi and capillary plugging. Development of ROS and high rates of apoptosis. Impaired oxygen delivery.
Contrast Nephropathy: A lot of discrepancy if this really exist. Generally, reversible cause. Risk of dialysis about 1%. Occurs about 2-4 days after exposure. Concerning patient groups would DM, cirrhotics, age, vascular disease, CKD. Mechanism poorly understood. Probably afferent vasoconstriction or free radical oxidation. Hold ace inhibitors prior to contrast. No evidence, but empirically tends to make sense. Bicarb and NAC for contrast - induced AKI is over, done, capute -- no benefit.