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Nephrology teaching round

52 M with alcoholism

SUBJECTIVE

Patient presents to Cortland

52 yo Male brought in by a caretaker to the ED

CC: Generalized weakness, poor appetite and jaundice.

HPI

- Brought in by his caretaker/daughter

- Lethargic

- Severe abdominal distension without pain

- At least a 'box' of wine a day for the past year

- No SOB, NVD, or fever

Past medical history

HTN

GERD

Paroxysmal A fib

OSA

Varicose veins of bilateral LE

Alcohol abuse

PMHx and Meds

Medications

Gabapentin 300 mg PRN

Losartan 50 mg QHS

Sotalol 80 mg BID

ROS

Positive for: -

Fatigue

Shortness of breath

Generalized weakness

ED course

ROS and ED course

Labs

Alk phos 392

AST/ALT 606/171

T bili 11.4

Direct bili 9

Infectious workup negative

Lactate 4.0 >> 5.3 (after 3 hours)

US abdomen

Hepatomegaly with steatosis, no convincing intrahepatic dilatation.

Images

A&P

To the ICU...

Acute on chronic alcohol intoxication/withdrawal

- CIWA

- GI consult

- PPI

Dehydration

- IV fluids

Elevated LFTs, secondary to ETOH abuse

- Trending down (???)

Generalized weakness

- PT/OT

Iron deficiency

- oral supplement when awake

Whole new A&P

a different hospitalist in the scene...

(She decided to intubate the patient and transfer him to RPH.)

1. Vent dependent respiratory failure

... turns out the patient was on precedex

X-ray - possible aspiration

- Empiric Abx broadened to Zosyn and vanco.

2. Metabolic encephalopathy

Infectious vs. possible liver failure.

Urgent GI consult

3. Sinus tachycardia with elevated D-dimer

- high risk for PE, on Lovenox

- CTA chest pending

4. Acute hepatitis superimposed on alcoholic cirrhosis

- Liver enzymes down but Tbili trending up.

Care at RPH ICU 12/20

Patient is transferred to RPH

Acute on chronic alcoholic hepatitis

Prednisolone 40 mg daily

CIWA

GI

PPI

Zosyn

AKI

Baseline Cr 0.6-0.9, p/w 1.3

UTI/Cystitis

Suspected psoas hemorrhage

Possible PE

Based on the possible etiologies...

Today's topic

Warrants a study of two topics.

Bile cast nephropathy

Hepatorenal syndrome

Additional pathophysiology...

The decline in kidney perfusion in this setting is associated with

- reductions in glomerular filtration rate (GFR)

- sodium excretion (often to less than 10 mEq/day in advanced cirrhosis)

- a fall in mean arterial pressure

Splanchnic vasodilatation = Significant.

Proved by response to ornipressin, an analog of antidiuretic hormone (arginine vasopressin)

= A preferential splanchnic vasoconstrictor

Hepatorenal syndrome's characteristics

Two types of HRS

HRS-AKI (type 1)

- x 2 increase in serum Cr. (i.e. 50% reduction in CrCl) within 2 weeks

- May be oliguric

Diuretic-resistant ascites (type 2)

- Ascites resistant to diuretics

- less serious than type 1

Dx of exclusion...

A prospective study from 2011

562 patients with cirrhosis and kidney function impairment

● Kidney injury associated with infection (e.g. sepsis or spontaneous bacterial peritonitis) – 46 %

● Prerenal acute kidney injury – 32 %

● Hepatorenal syndrome – 13 %

● Parenchymal kidney disease (such as glomerulonephritis) – 9 %

Tx

- Stop antihypertensive agents, including beta-blockers

- If in ICU, use norepinephrine + albumin. (Norepinephrine 0.5 - 3 mg/hr, to raise the MAP by 10 mmHg. Albumin for 2 days, 1g/kg per day, 100g = max)

IV vasopressin may also be effective

- If NOT in ICU, terlipressin (IV, 1-2mg Q4-6H) + albumin.

If terlipressin NOT available, midodrine, octreotide and albumin.

- If medical Tx fails, Transjugular Intrahepatic Portosystemic Shunt... too many complications.

- Or... DIALYSIS and then transplant.

El Chediak, A., Janom, K. & Koubar, S.H. Bile cast nephropathy: when the kidneys turn yellow. Ren Replace Ther 6, 15 (2020). https://doi.org/10.1186/s41100-020-00265-0

Patel, J., Walayat, S., Kalva, N., Palmer-Hill, S., & Dhillon, S. (2016). Bile cast nephropathy: A case report and review of the literature. World Journal of Gastroenterology, 22(27), 6328.

Van Slambrouck, C. M., Salem, F., Meehan, S. M., & Chang, A. (2013). Bile cast nephropathy is a common pathologic finding for kidney injury associated with severe liver dysfunction. Kidney international, 84(1), 192-197.

Soman, S., Aurora, L. (2021). Type 3 Cardiorenal Syndrome. In: McCullough, P.A., Ronco, C. (eds) Textbook of Cardiorenal Medicine. Springer, Cham. https://doi.org/10.1007/978-3-030-57460-4_9

https://healthjade.net/portal-vein/

https://www.uptodate.com/contents/hepatorenal-syndrome?search=hepatorenal%20syndrome&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1

Stocker, R., Yamamoto, Y., McDonagh, A. F., Glazer, A. N., & Ames, B. N. (1987). Bilirubin is an antioxidant of possible physiological importance. Science, 235(4792), 1043-1046.

https://www.microscopyu.com/techniques/polarized-light/principles-of-birefringence

Ziberna, L., Martelanc, M., Franko, M., & Passamonti, S. (2016). Bilirubin is an endogenous antioxidant in human vascular endothelial cells. Scientific reports, 6(1), 1-6.

Sources

Nephrology consult on 12/22

AKI on CKD III

Etiology:

- Prerenal

- Possible hepatorenal

- Contrast-induced

- Bilirubin induced ATN

Nephrology onboard

Assessment

AKI on CKD III

Baseline Cr 0.7, p/w 1.3 >> 1.5

Volume status: Euvolemic

Electrolytes: Stable

Blood pressure: WNL but soft

Hb: stable at 9.2, anemic

The recommendations

- LR 75 cc/h x 12hours

- 25% albumin q8h for 1 day

- Urine electrolytes

- Urine microscopic analysis

Plan

Renal function

Day 2-4 f/u

Day 5 f/u

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