AKI April 15th

On april 15th we talked about a patient with an elevated Creatinine of 600.

The discussion of acute vs chronic was brought up the day prior as well.

Some tips that MAY help us.

1. And old creatinine (easy enough), seeing a creatinine that was much lower 1 week prior.
2. Anemia - this is quite simply due to the fact that erythropoeitin is produced in the peritubular capillary cells in the kidneys, and with chronic damage, patient's become anemia. We generally target Hb between 100-110 in a patient with CKD. Trials have been done (although underpowered - CREATE and COIR) to try to demonstrate a benefit of increasing Hb levels - there was a trend to increasing mortality. Note** patients with polycystic kidney disease typically have EPO spared and so not as anemia!
3. Hypocalemia - the 1 alpha hydroxylase in vit D is produced in the proximal tubular cells of the kidney, hence patient may be low in activated Vit D.
4. Shrunken kidneys -  8 cm or less is generally used. This want be for ALL kidney disease but most commonly associated with hypertension.
5. Bone disease - are increased risk of bone disease because of high PTH and presumably high bone turnover. They may also be at risk of vascular calcification (within coronary arteries and even aortic stenosis - note KDIGO guidelines don't recommend to routinely screen for this, i.e. with echo)

Above is the classic breakdown of approach to acute renal failure. Thinking about the causes can seem overwhelming, best to start with the potentially easier things to diagnose and fix, and then some red flags to look for for RENAL causes.

Pre-renal is the majority of AKI we seen in the hospital in patients that are admitted. Looking for a history of dehydration, nausea/vomiting, diarrhea. A simple urine lyties and urine osm will put us in the right direction!

Urine sodium <20

urine osm >500 

Signs of a kidney that is trying to reabsorb sodium (and water to follow) and where ADH is increased hence concentrating the urine. Urine specific gravity is a simple way to pick up pre-renal and when the story for pre-renal is a good one a urinalysis would probably all that needed. 

How do we treat it? with fluids! The most important thing to consider is what will kill the patient first which is hyperkalemia, but those reading the blog are already pros at that!

As we see prenreal most commonly in hospital: and we order urine lytes quite often, its important to think of some situations that can cause a false negative result; high urine sodium in the setting of prerenal

1. Diuretic use, there job is prevent sodium reabsoption, thereby possibly elevated the urine sodium results.. keeping in mind that the lasix may have done this in the first place

2. underlying CKD: patients may have baseline poor abilities to reabsorb sodium

3. After IV fluids; this has been reported and may be related to a large sodium and maxing out our kidneys ability to reabsorb all of it

4. Glucosuira - osmotic pull telling water and electrolytes with it

5. Salt wasting disorders: adrenal insufficiency - lack of aldosterone will prevent sodium reabsorption in the DCT.

The above discussion although interesting, may be impractical. If someone comes in tachycardic, hypotensive, with dry mucous membranes, flat neck veins, low cap refill in the setting of nausea and vomiting from a partial bowel obstruction - screaming at you "I'm thirsty!"...they are dehydrated, the urine lytes wouldn't really matter.

Post renal causes: anything post kidney is a post renal cause - including renal pelvis, but remember we need bilaterally obstruction. So when do we go searching for this? when patients aren't making sufficient urine, 0.5ml/kg/hr (<500 per day) despite fluids, we need to consider obstructive causes. The easier thing is to insert a foley (with plans to remove it within 24 hours if things go accordingly) or a bladder scan. 

Seeing no urine with the above may move one to consider higher up obstruction. The reason this is important to pick up sooner than later is because we can do something about it! Whether this is by-passing the prostate with a suprapubic catheter, or bilateral nephrostomy tubes in the renal pelvices.

Renal causes:

Acute tubular necrosis: muddy brown casts are pathognomonic and something we do not want to see. >10 per high power field has the best specificity. This happens in response to prolonged ischemia (pre-renal for a long time) and toxins!

endogenous - uric acid (tumor lysis), lytes chains in multiple myeloma, and rhabdo!

exogenous - drugs, aminoglycosides, contrast

The urine sodium will be elevated as the kidney has lost its concentrating ability. This may take 2-3 weeks to recover, but some patients may go on to develop CKD.

AIN: most commonly associated with drugs, infection, may see eosinophiluria in the urine although not very sensitive, or sterile pyuria. Remove the agent.. treat the infection, debatable about using steroids.

RBC casts:This is something you need to look for, but do not want to see. This leads us down the pathway of glomerulonephritis, is this a type of vasculitis and that's when a detailed review of systems will be considered.

TTP/HUS: schistocytes, increased creatinine, and thrombocytopenia the dreaded renal disease as the mortality is extremely high without PLASMAPHERESIS, which essentially filters out antibodies to ADAMTS13. Which is though to be deficient in these individuals.

Does everyone with increased creatinine need an ultrasound?

NO

think about what will be done with that information, if you believe this is all pre-renal, see how they recover it maybe useful to consider in the future for assessing for CKD if there creatinine doesn't recover. 

However, if you think there is obstruction this should get done - potentially overnight.

Commonly we would be looking for hydro on the renal ultrasound acutely

be aware of some false negatives!

4 settings!

1. with very early obstruction <8 hours

2. when the patient has obstruction but is also volume depleted - may consider repeating the test after fluids

3. retroperitoneal fibrosis, may cause hydronephrosis without ureteral dilatation; the hydro and fibrosis is best seen on CT scan

4.  with mild obstruction, as to not impair renal function.

The classic clerk question: what are the indications for dialysis?

AEIOU

acidosis - refractory to medical therapy, i.e. shifting

electrolyte (hyperkalemia) - refractory to medical therapy

ingestions - aspirin, lithium are common ones

overload - someone who is on dialysis or is not making uring and is volume overloaded

uremia - pericarditis, encephalopathy