Hemodynamics & Ascites
This vascular change in the splanchnic circulation is the root hemodynamic driver of ascites and renal failure in cirrhosis.
What is splanchnic vasodilation?
This PMN count in ascitic fluid is the diagnostic threshold for SBP, even with a negative culture.
What is ≥ 250 PMNs/mm³?
This type of cast seen on urinalysis is pathognomonic for ATN and was notably absent in James Cooper's urine.
What are muddy-brown granular casts?
HRS Type 1 (HRS-AKI) is defined by a rapid doubling of creatinine to above this threshold within 2 weeks.
What is 2.5 mg/dL?
This is the FENa formula, where U = urine, P = plasma, Cr = creatinine, Na = sodium.
What is FENa = (U_Na × P_Cr) / (P_Na × U_Cr) × 100?
Despite massive ascites and edema, the kidney in cirrhosis behaves as if the patient is volume-depleted because of a fall in this specific parameter.
What is effective arterial blood volume (EABV)?
This is the mechanism by which gut bacteria enter the peritoneum in SBP without a visible perforation.
What is bacterial translocation?
A urine sodium of 5 mEq/L and urine osmolality of 1600 mOsm/kg together indicate that the tubules are doing this.
What is actively reabsorbing sodium and water (tubular function is intact)?
This is the key clinical feature that distinguishes HRS-AKI from simple prerenal azotemia in a cirrhotic patient.
What is failure to improve after 48 hours of adequate volume expansion with albumin?
Albumin's role in SBP/HRS is not simply oncotic. It also acts through this additional mechanism that explains why it reduces HRS risk beyond what saline can achieve.
What is binding and neutralizing circulating bacterial products, cytokines, and inflammatory mediators?
These three neurohormonal systems are activated in cirrhosis in response to arterial underfilling and collectively drive sodium retention, water retention, and renal vasoconstriction.
What are RAAS, the sympathetic nervous system (SNS), and ADH?
This is the name given to SBP in which the ascitic PMN count exceeds the diagnostic threshold but cultures return negative, as seen in James Cooper's case.
What is culture-negative neutrocytic ascites?
In ATN, tubular injury causes the urine osmolality to approximate this value, a state called isosthenuria.
What is ~300 mOsm/kg?
HRS Type 2 differs from HRS Type 1 in this way regarding tempo and its typical clinical association.
What is a slower, more gradual decline in renal function (chronic), most often associated with refractory ascites rather than acute decompensation?
This is why FENa is unreliable for diagnosing prerenal AKI in a patient already taking loop diuretics, and what alternative index should be used instead.
What is that diuretics force urinary sodium excretion regardless of volume status, falsely elevating FENa — FEUrea (< 35% suggests prerenal) is preferred?
In cirrhosis, non-osmotic release of this hormone causes water retention that exceeds sodium retention, producing dilutional hyponatremia.
What is ADH (vasopressin)?
In addition to antibiotics, this intervention given on day 1 and day 3 is proven to reduce HRS incidence and improve survival in SBP.
What is intravenous albumin?
James Cooper's creatinine rose from 0.7 to 2.5 mg/dL. In a cirrhotic patient, this feature of creatinine metabolism means the true GFR decline is even worse than the number suggests.
What is reduced creatinine production due to decreased muscle mass and impaired hepatic creatine synthesis?
This is why liver transplantation is considered the definitive treatment for HRS, rather than any renal-directed therapy.
What is that transplant corrects the underlying portal hypertension and hemodynamic failure that drives renal vasoconstriction — the kidney itself is structurally normal?
Midodrine is an alpha-1 agonist given orally in HRS. This is its mechanism of action and why it improves renal perfusion in the setting of splanchnic vasodilation.
What is that it causes systemic vasoconstriction, raising SVR and mean arterial pressure, thereby counteracting splanchnic vasodilation and redistributing blood flow to the kidneys?
This endogenous vasodilator, overproduced in response to portal hypertension, is the primary mediator of splanchnic vasodilation and the initiating step in the HRS cascade.
What is nitric oxide (NO)?
SBP precipitates HRS through this mechanism — linking bacterial products to worsened splanchnic vasodilation and renal failure.
What is systemic release of inflammatory cytokines (TNF-α, IL-6) causing worsened vasodilation and further reduction in effective arterial volume?
This is the AKI subtype in which urine sodium is low, urine osmolality is high, and sediment is bland, yet the kidney fails to recover despite adequate volume resuscitation with albumin.
What is hepatorenal syndrome (HRS-AKI)?
These are the four diagnostic criteria that must be met to diagnose HRS-AKI in a cirrhotic patient.
What are: (1) cirrhosis with ascites; (2) AKI by creatinine criteria; (3) no improvement after 48h albumin + diuretic withdrawal; (4) absence of shock, nephrotoxins, structural kidney disease, or obstruction?
Ceftriaxone is the antibiotic of choice for SBP. Name two contraindications or major precautions and explain why norepinephrine is used as a vasoconstrictor in HRS rather than simply giving more IV fluids.
What are: hypersensitivity to cephalosporins/penicillins (cross-reactivity); caution in neonates with hyperbilirubinemia. NE is used because the problem is vasodilation — adding more fluid worsens ascites without fixing vascular tone; NE directly raises SVR and renal perfusion pressure.