Overview of Kidney Disease & Nephrotoxicity 2024

functional unit of the kidney

nephron: Glomerulus, Proximal tubule, Loop of Henle, Distal Tubule, Collecting Duct

Label it this is the first question on the exam

Describe the flow of blood through the kidney.

Blood enters the kidney through the renal artery, flows into the glomerulus for filtration, and exits via efferent arterioles. Filtered blood moves through peritubular capillaries or the vasa recta to exchange substances, then exits the kidney through the renal vein.

Distinguish between filtration, secretion, and reabsorption

Filtration removes small molecules from the blood into the nephron, reabsorption returns essential substances to the blood, and secretion adds waste and excess ions to the filtrate for excretion.

Three causes of AKI

Pre renal
Post renal
Intrinsic (Parenchymal)

Pre renal AKI Def

• Decreased perfusion to the kidneys 

• No intrinsic damage to kidneys yet

• Low fractional excretion of sodium

Causes of Pre Renal AKI

Volume depletion
Hypotension
Edematous States
Renal Ischemia

Intrinsic Disease Def

Kidney itself is damaged

Causes of Intrinsic Disease

Glomerular Damage
Vascular Damage
Acute tubular nectosis - constrast dyes, toxins
Acute interstitial nephrtitis - NSAIDs, PPIs, Infections

Post Renal Disease Def

-Obstructive uropathy

Hydronephrosis: urine builds up in the kidneys, causing them to swell and stretch

Causes Post Renal Disease

Bladder outlet obstruction
Renal obstruction
Ureteral obstruction

Compare specific gravity for the 3 types

	Pre renal	Intrinsic	Post renal
Specific Gravity	High >1.020	Normal 1.008-0.012	Low <1.015

Compare BUN: Scr for the 3 types

	Pre renal	Intrinsic	Post renal
BUN: SCr	>20:1	10:1	<20:1

Compare urine sodium for the 3 types

	Pre renal	Intrinsic	Post renal
Urine sodium	Low <20	>40-50	>40

Compare FeNa for the three types (fractional excretion of Na)

	Pre renal	Intrinsic	Post renal
FENa	< 1%	>2%	>1% but variable

Nephrotoxins

Acute tubular necrosis- contrast dyes, aminoglcosides
Hemodynamic changes- ACEI, NSAIDs, Tacrolimus, Cyclosporine
Acute insterstitial nephritis- Penicillins, cephalosporins, Lithium, PPIs
Obstruction
Acyclovir

Risk factors for Constrat dye AKI

CKD
DM
Dehydration

Prevention of COntrast dye AKI

-Non ionic low osmolal ir iso osmolal contrast agents
-Prehydration
-STOP metformin, NSAIDs, ACEIs, diuretics

How to manage ACEI,ARB AKI

-May restart ACEI/ARB at lower dose

How to manage penicillin AKI

stop and do not retry

How to manage Acyclovir AKI

stop drug and hydrate