Renal Tubular And Interstital Diseases Flashcards Preview

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Flashcards in Renal Tubular And Interstital Diseases Deck (19)
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Acute Pyelonephritis

Tubular interstitalnephritis caused by a bacterial infection in the renal pelvis

Usually caused by UTIs and affects either the upper or lower urinary tract
- most common is the lower urinary tract (most dont go to the kidney though)
- can also be hematogenous, but most common is ascending via the lower urinary tract
- ** under normal conditions, the urine can kill the bacteria, however in pyelonephritis, outflow obstruction or bladder dysfunction is usually secondary and sets the stage for the UTI and subsequent pyelonephritis**

Most common causes
- E.coli
- PPEcKS species (enteric gram (-) bacilli)

- sudden pain at the costovertebral angles
- chills/fever/nausea malaise
- dysuria and urgency to urinate
- urine contains pus and looks frothy


Tubular interstital nephritis (TIN) causes

Is inflammation of the tubular vessels

Tubular injury via:
- drugs
- metabolic disorders
- hypokalemia
- irradiation
- viral infections
- immune reactions

**these are NON-bacterial casues, since bacterial causes = pyelonephritis**


What is one of the most important physiological causes of ascending acute pyelonephritis?

Incompetence of the Vesicoureteral orifice resulting in a reflex contraction (allows the bacteria to ascend the ureter)
- this reflex (VUR) is present in 20-40% of young a children with UTIs (usually via flaccid bladder, spinal cord injury, diabetes, congenital defective valve)



Pyelonephritis with prominent obstruction which prevents pus from draining at all within the kidney


Papillary necrosis

A rare complication of pyelonephritis that has 3 predisposing conditions
- diabetes
- urinary tract obstruction
- sickle cell anemia

**shows ischemic and suppurations necrosis of the tips of the renal pyramids**


Chronic pyelonephritis

Pyelonephritis what shows interstitial inflammation and scarring of the renal parenchyma
- also history of urinary tract infections And recurrent obstructive lesions
- most commonly is unilateral, but could be bilateral (only congenital abnormalities usually though)

Two forms:
1) chronic obstructive pyelonephritis
- caused by recurrent infections superimposed on obstructive lesions in the kidney

2) chronic reflux-associated pyelonephritis
- ***most common cause of chronic pyelonephritis***
- results from superimposition of a UTI on congenital VUR and intrarenal reflux


Chronic pyelonephritis morphology

Shows blunting of the calyxes and uneven scarring of the pelvis and calyces

Calcifications in kidneys as well

- very slow growing and usually only caught by routine labs, development of new HTN or gradual increases in signs for CKD
- CKD signs and dysuria are the most common but symptoms vary widely


Drug-induced tubulointersitial nephritis (TIN)

Most common
- rifampin
- penicllins**
- PPIs
- NSAIDs**
- cimetidine
- loop diuretics (furosemide)
- etc.
** = most common

Is believed to be caused by the drugs acting as haptans for the host immune system when combined with tubular cells in the kidneys
- is IgE/ T-cell mediated immune reactions
- always shows abundant eosinophils and neutrophils


Clinical features of drug-induced TIN

Begins 15 days after exposure to the drug
- characterized by new onset of fever, eosinophila, edema and renal abnormalities
- also hematuria, proteinuria and leukocyturia (but this varies on amount)

50% of cases show rising serum creatinine or acute kidney injury with ologuria

Treatment = symptomatic treatment and remove offending agent


Acute tubular injury/necrosis (ATI)

Characterized by damage to the tubular epithelial cells and an acute decline in renal function
- often presents with granular casts
- often presents with oliguria (low urine output)

Shows decreased GFR and concurrent elevation of serum creatinine

** ATI’s are the most common cause of acute kidney injuries**


Two forms of acute tubular injury/necrosis

1) ischemic acute tubular injury
- inadequate blood flow to all or some peripheral organs (shock, severe trauma, blood loss, acute pancreatitis, sepsis)
- additional causes = Microscopic polyangitis, malignant HTN and thrombotic microganipathies
- * usually damages PCTs and TAL

2) nephrotoxic acute tubular injury
- chronic exposure to heavy metals, poisons, organic solvents,antibiotics or radiographic contrast


What tubular cells are most sensative to hypoxemia and toxins?

Proximal tubular epithelial cells (PCT) and the TAL


How does repair of ATI/ATN occur?

The tubular necrosis and disabled integrity of the basement membrane can be reversed IF the cause is fixed/removed


Fanconi syndrome

Reabsoption defect in the PCT
- causes increased excretion of amino acids, glucose, HCO3- and Phosphate

Leads to metabolic acidosis, hypophosphatemia and osteopenia

Casues = Wilson’s disease, hers disease, multiple myeloma, nephrotoxic drugs, lead poisoning


Bartter syndrome

Reabsoption defect in the TAL which effects the N/K/2Cl channels

Results in metabolic alkalosis, hypokalemia and hypocalcinuria

Causes = autosomal recessive inheritance

**looks similar to chronic loop diuretic use**


Gitelmann syndrome

Reabsoption defect of NaCl in the DCT

Results in metabolic alkalosis, hypomagnesemia, hypokalemia, hypocalcinuria

Caused by autosomal recessive inheritance

**looks similar to thiazide diuretic abuse**


Liddell syndrome

Gain of function mutation in ENaC channels of the collecting duct
- increases sodium reabsorption

Results in metabolic alkalosis, hypokalemia, HTN and decreased aldosterone levels

Casues are autosomal dominant inheritance

**looks very similar to hyperaldosteronism but aldosterone levels will be near 0**
- treat with amiloride


Syndrome of apparent mineralocorticoid excess

Deficency in 11B-HSD receptors
- these receptors turn off cortisol by turning into cortisone (inactivated form) so results in cortisol levels being elevated and mimicking hyperaldosterone effects

Leads to metabolic alkalosis, hypokalemia, HTN, and hypernatremia and decreased serum aldosterone

**caused by autosomal recessive inheritance and over consumption of licorice( over production of glycrrhetinic acid) **

Treatment = K+ sparring diuretics


What structure abnormalities does ischemia lead to in tubular epithelial cells?

Loss of cell polarity (reversible)
- causes redistribution of membrane proteins from basolateral to luminal surface

Loss of PCT ability to reabsorb sodium

Afferent arteriolar vasoconstriction and decreased GFR