Thread by @zachary_c_owens

Hey #MedStudentTwitter, I am on inpatient nephrology consults for the next month and wanted to share some of the teaching pearls I learn each day. So, I decided to start this threat! I will add more every couple of days.

Hope y’all find it helpful!

Teaching point 1:

When documenting the dialysis plan, nephrologists like the following to be included:

(1) nephrologist managing their outpatient dialysis, (2) dialysis center, (3) dialysis schedule and duration of each session, (4) estimated dry weight and goal weight.

Teaching point 2:

In patients with AKI, FENa really only matters if they are oligiric (UOP < 400 mL), otherwise it’s essentially useless.

If a patient with oligiric AKI is on diuretics (loops or HCTZ) then FENa will be falsely elevated. FEUrea is preferred here.

Teaching point 3:

I’m patients with acute on chronic kidney injury who require dialysis, baseline renal function is the best predictor of whether or not they will require dialysis permanently. Those with CKD 4 or 5 are at highest risk.

Teaching point 4:

Hepatorenal syndrome management consists of (1) midodrine (increases SVR), (2) octreotide (splanchic vasoconstriction) and (3) albumin (pulls fluid back into intravascular space). Net effect of all of these is increasing renal perfusion.

Teaching point 5:

GFR estimates are not accurate in the setting of AKI.

Teaching point 6:

Hyaline casts are empty shells of Tamm-Horsfall protein that form when there is slowed flow through renal tubules. Usually seen in pre-renal AKI and dehydration.

Note: these cells form the base/scaffold for all other casts that can be seen in urine sediment

Teaching point 7:

RBC casts + dysmorphic RBC = glomerulonephritis

WBC casts = inflammation of renal interstitial classically seen in (1) pyelonephritis and (2) AIN

Granular casts = necrotic tubular epithelial cells = acute tubular necrosis

Fatty casts = nephrotic syndrome

Teaching point 8:

You don’t need to avoid nephrotoxic agents (aminoglycosides, IV contrast, etc) in patients with ESRD since they are dialysis dependent. There renal function cannot get any worse, so these agents are generally not avoided.

Teaching point 9:

Patients with a GFR < 30 should not be given gadolinium contrast due to increased risk of nephrogenic systemic sclerosis.

Teaching point 10:

30,000 ft view of dialysis modalities:

Intermittent HD: 3x/wk, 3-4 hrs, classic dialysis, efficient but high stress on hemodynamics

SLED: in between IHD and CRRT

CRRT: 24/7, common in ICU, lower efficiency but lower stress on hemodynamics

Teaching point 11:

Hypotonic hypervolemic hyponatremia has three major etiologies: CHF, cirrhosis, nephrosis

Common thread = low ECV ➡️ non-osmotic release of ADH ➡️ increased free water reabsorption in CD, esp w/ ⬆️ water intake

Another similarity = high Uosm (>100)

Teaching point 12:

Anatomical Approach to Intrinsic AKI:

Glomerulus: GN
Tubules: ATN or obstruction (MM)
Interstitium: drugs, infection, immune
Vascular: MAHA, CH emboli, scleroderma renal crisis

Credit: @CPSolvers

Teaching point 13:

Cardiorenal syndrome (CRS) can occur in situations other than ADHF, cardiogenic shock, and ACS. When any these leads to AKI, that is know as Type 1 CRS, which is the classic CRS picture most people have.

That, however, is not the only type of CRS.

Teaching point 14:

CRS can occur when ⬇️CO leads to ⬇️ renal perfusion.

T1 CRS = acute ⬇️ CO leads to AKI
T2 CRS = chronic ⬇️ CO leads to progressive CKD

Teaching point 15:

CRS can also occur when ⬇️ renal function affects ❤️ function.

T3 CRS = acute ⬇️ renal fxn (AKI, GN) ➡️ acute ❤️ dysfxn (⬆️K=arrhythmia)

T4 CRS = chronic ⬇️ renal fxn ➡️ chronic ❤️ disease (diastolic dysfunction)