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Flashcards in Renal Deck (144)
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Clinical Case:

A 81 year old man presents to his PCP with complaints of frequent urination, rash, and fever.  Blood labs show eosinophilia.  U/A shows proteinuria.  Imaging shows edema and lymphocytes inside the tubules.  The patient notices that the rash appears whenever he takes his thiazide diuretic.

what does this man have?

Acute Drug-Inducd Interstitial Nephritis


Analgesic Nephropathy

  • chronic renal disease caused by excessive intake of analgesic mixtures and having chronic  tubulointerstitial nephritis and renal papillary necrosis.
    • usually phenacetin, aspirin, caffeine, acetaminophen, and codeine.  usually two of them.
  • sequence of events: papillary necrosis, then cortical tubulointerstitial nephritis from impeded urine flow.  also water depletion
    • phenacetin's metabolite = acetaminophen ⇒ depletes cells of glutathione ⇒ oxidative metabolites
    • aspirin ⇒ inhibits vasodilation from prostaglandins ⇒ ischemia for papillae
  • morphology: kidneys normal or slightly small, depressed areas of cortex = cortical atrophy over necrotic papillae.
    • papillae show stages of necrosis, calcification, fragmentation, and sloughing.
    • early = patchy necrosis.  late = entire papilla necrotic ⇒ ghosts of tubules and foci of dystrophic calcification.
    • cortical changes = atrophy of tubules, interstitial fibrosis and inflammation.  cortical columns of Bertin are spared atrophy.
  • presentation: more common in women (5:1).  prevalent in people with recurrent headaches and muscle plain, psychoneurotic patients, and factory workers.
    • early findings = hyposthenuria (can't concentrate urine) and distal tubular acidosis ⇒ kidney stones.
    • symptoms = headache, anemia, GI symptoms, and HTN.  50% have UTI. can have hematuria or renal colic if ureter obstructed.
    • MRI and CT show papillary necrosis and calcifications.
    • can progress to transitional papillary carcinoma of the renal pelvis.
  • tx: drug withdrawal can cause stabilization or improvement.  


Clinical Case:

A 46 year old female presents to her PCP with a complaint of prolonged diarrhea and stomach ache and a headache for the past week.  She has a history of recurrent headaches and kidney stones.  She is currently taking phenacetin and aspirin but it is not reducing her pain level very much.  U/A shows a specific gravity of 1.010.  CT shows calcification and necrosis in the papillae.  Biopsy reveals the papillae are at varying stages of necrosis, calcification, and sloughing.

What does this patient most likely have?

Analgesic Nephropathy


Nephropathy Associated with NSAIDs

  • adverse effects related to ability to inhibit COX-dep PG synthesis.  COX-2 is in kidney.
  • related syndrome: acute renal failure from ↓ blood flow; acute hypersensitivity interstitial nephritis; acute interstitial nephritis and minimal change disease; membranous nephropathy.


Aristolochic Nephropathy

  • chronic tubulointerstitial nephritis from aristolochic acid found in herbal remedies.
  • forms adducts with DNA ⇒ renal failure and interstitial fibrosis associated with paucity of infiltrating leukocytes.
  • increased incidence of carcinoma of kidney and urinary tract.


Clinical Case:

A 62 year old female presents to the ER for sudden appearance of blood in her urine.  She takes herbal supplements and teas every winter to ward off the flu and any colds.  U/A reveals hematuria and moderate proteinuria.  Biopsy of her kidney reveals interstitial fibrosis but few leukocytes.

What does she have?

Aristolochic Nephropathy


Urate Nephropathy

  • 3 types:
    • 1. acute uric acid nephropathy = from precipitation of uric acid crystals in renal tubules, mostly collecting duct ⇒ obstruction of nephrons ⇒ acute renal failure
      • common in those with leukemias and lymphomas with chemo
    • 2. chronic urate nephropathy = gouty nephropathy = protracted forms of hyperuricemia.  deposition of monosodium urate crystals in acidic milieu of distal tubules and collecting ducts and interstitium.  may form birefrinent needle-like crystals in tubular lumens or interstitium.
      • tophus = made of foreign-body giant cells, mononuclear cells, firbotic rxn.
      • tubular obstruction ⇒ cortical atrophy and scarring.
      • renal arterial and arteriolar thickening from HTN.
      • may have increased exposure to lead from moonshine.
    • 3. nephrolithiasis = uric acid stones. in 22% of those with gout, 42% of those with secondary hyperuricemia.


Clinical Case:

A 38 year old male presents to the ER with pain and swelling in his joints.  He says he has gout and has had this many times before.  He has also been complaining of  weakness and nausea.  He was diagnosed with HTN a few years ago.  U/A shows microscopic hematuria and proteinuria.  Biopsy of the kidneys reveals deposits of monosodium urate crystals in the distal tubules, collecting ducts, and interstitium.  On IF there are birefringent needle-like crystals in the interstitium.

What does he have?

Chronic Urate Nephropathy



  • associate with hypercalcemia as found in hyperparathyroidism, multiple myeloma, vitamin D intoxication, metastatic cancer, and excess calcium intake (milk-alkali syndrome).
  • is deposition of calcium in kidney's or calcium stones.
  • can cause chronic tubulointerstitial disease and renal insufficiency.
  • earliest damage done to tubular epithelial cells from mitochondrial distortion.
  • then deposits appear in mitochondria, cytoplasm, basement membrane.
    • can obstruct  tubular lumen ⇒ atrophy of nephrons and 2° interstitial fibrosis and inflammation.
    • have alternating areas of scarred and normal parenchyma.
  • earliest functional defect is inability to concentrate urine.  can also get tubular acidosis and salt-losing nephritis.  
  • slowly progresses to renal insufficiency


Acute Phosphate Nephropathy

  • excessive accumulation of calcium phosphate crystals in tubules.
    • in patients consuming high doses oral phosphate (for colonoscopy)
    • NOT HYPERCALCEMIC.  have excess phosphate load.  dehydration can ⇒ precipitation of calcium phosphate ⇒ renal insufficiency a few weeks later.
  • only partially recover renal function.


Clinical Case:

A 55 year old male presents to his PCP with a complaint of ongoing nausea and urinating less than normal.  He has been feeling this way for the last 2 weeks, since he had his colonoscopy done.  Renal biopsy reveals accumulations of calcium phosphate crystals in his tubules.

what does he have?

Acute Phosphate Nephropathy


LIght-Chain Cast Nephropathy

  • aka myeloma kidney.
  • is tubulointerstitial from tumor (hypercalcemia, hyperuricemia, obstruction of ureters) or therapy (irradiation, hyperuricemia, chemo, infections).
  • in multiple myeloma:
    • Bence Jones proteinuria and cast nephropathy.  failure = amount Bence Jones protein. combine with Tamm-Horsfall protein in kidney under acidic conditions to form large distinct tubular casts that obstruc tubular lumens and cause inflammation around casts.
    • amyloidosis - AL type
    • light-chain deposition disease: kappa type light chains deposit in GBMs and mesangium in nonfibrillar forms, ⇒ glomerulopathy, or in tubular basement membrane ⇒ tubulointerstitial nephritis.
    • hypercalcemia and hyperuricemia.
  • morphology: pink or blue amorphous masses (Bence Jones tubular casts) distend lumen. surrounding multinucleate giant cells from phagocytes.  interstitial tissue has nonspecific inflammation and fibrosis.  sometimes get granulomatous rxn.
  • presentation: chronic renal failure develops insidiously (most common).  
    • acute renal failure with oliguria.  
    • precipitating factors: dehyrdation, hypercalcemia, acute infection, treatment with nephrotoxic antibiotics.
    • Bence Jones proteinuria in 70% multiple myeloma.
    • non-light-chain proteinuria suggests amyloidosis or light-chain deposition disease.


Clinicl Case:

A 47 year old female presents to her PCP for routine followup of her multiple myeloma.  Her U/A reveals  Bence Jones proteinuria.

What does she hae and what would you expect her biopsy to reveal?

She has Light-Chain Cast Nephropathy.

Expect her biopsy to show interstitial inflammation and fibrosis, Bence Jones casts with multinucleate giant cells around them.


Benign Nephrosclerosis

  • renal pathology associated with sclerosis of renal arterioles and small arteries.
  • focal ischemia by vessels with thickened walls and narrowed lumens
  • parenchymal effects: glomerulosclerosis, chronic tubulointerstitial injury ⇒ ↓ functional renal mass.
  • more frequent in blacks, HTN, diabetes mellitus.
  • have medial and intimal thickening and hyaline deposition in arterioles from extravasation of plasma proteins in injured endothelium and ↑ deposition of basement membrane matrix.
  • morphology: kidneys normal or slightly smaller, fine granularity (grain leather) of cortex.
    • hyaline arteriolosclerosis of small arteries and arterioles
    • microscopic subcapsular scars with sclerotic glomeruli and tubular dropout.
    • fibroelastic hyperplasia = interlobular and arcuate arteries have medial hypertrophy, reduplication of elastic lamina, and ↑ myofibroblastic tissue in intima ⇒ narrowed lumen.
    • narrowing ⇒ patchy ischemic atrophy
      • foci of tubular atrophy and interstitial fibrosis
      • collapse of GBM, deposition of collagen in Bowman space, periglomerular fibrosis, and total sclerosis of glomeruli.
  • Presentation: moderate ↓ renal blood flow, normal GFR or slightly reduced. may have mild proteinuria
    • ↑ risk renal failure in: African Americans, HTN, diabetes mellitus


Malignant Nephrosclerosis

  • associated with malignant or accelerated phase of HTN.
    • often superimposed on preexisting essential benign HTN, 2° forms HTN, or underlying chronic renal disease (GN or reflux nephropathy)
    • frequenct cause of death from uremia in pts with scleroderma.
    • usually young, men, black.
  • pathogenesis: initial insult is vascular damage to kidney (long-standing HTN, arteritis, coagulopathy)
    • ⇒ ↑ permeability of small vessels to fibrinogen and plasma proteins, endothelial injury, focal death of vascular wall cells, platelet deposition ⇒ fibrinoid necrosis of arterioles and small arteries, swelling of vascular intima, intravascular thrombosis.
    • PDGF, plasma, and other cells ⇒ hyperplasia of intimal smooth muscle cells ⇒ hyperplastic arteriolosclerosis.
    • kidney becomes very ischemic ⇒ very ↑ plasma renin levels, ↑ aldosterone levels.
    • all adds up to cuse malignant arteriolosclerosis
  • morphology: small pinpoint petechial hemorrhages on cortical surfaces = 'flea-bitten' appearance.
    • fibrinoid necrosis of arterioles - eosinophilic granular change in blood vessel wall.
    • onion-skinning = intimal thickening by proliferating smooth muscle cells and accumulation of plasma protein and proteoglycans around blood vessel = hyperplastic arteriolitis
  • presentation: systolic pressure > 200 and diastolic > 120, papilledema, retinal hemorrhages, encephalopathy, cardovascular abnormalities, renal failure.
    • early symptoms: headaches, nausea, vomiting, visual impairments (scotomas aka spots)
    • HTN crises: loss of consciousness or convulsions.
    • marked proteinuria and hematuria
  • tx: anti-HTN drugs, this is a medical emergency.


Clinical Case:

A 24 year old African American male presents to the ER after suddenly losing consciousness in a grocery store.  He currently complains of a headache, nausea, and seeing spots.  His b/p is 210/125.  His U/A reveals proteinuria and microscopic hematuria.  Blood labs reveal ↑ levels of renin and aldosterone.  Biopsy of his kidney reveals onion-skinning around the arterioles as well as fibrinoid necrosis.

What does this man have?

Malignant Nephrosclerosis


Renal Artery Stenosis

  • unilateral = 2-5% HTN
  • from stimulation of renin secretion by JGA and production of angiotension II
  • morphology: 70% from occlusion by atheromatous plaque at origin of renal artery. more in men and increases with age and diabetes mellitus.  concentrically placed with superimposed thrombosis.
    • 2nd type = fibromuscular dysplasia of renal artery.  fibrous and fibromuscular thickening involving intima, media, or adventitia.  medial is most common.  more common in women, age 20-40.   usually medial or distal part of renal artery. can involve segmental branches and be bilateral.
    • ischemic kidney is small with atrophy, crowded glomeruli, atrophic tubules, interstitial fibrosis, focal inflammatory infiltrates.  unaffected kidney has more severe arteriolosclerosis from HTN.
  • presentation: resemble essential HTN.  may hear bruit in affected kidneys.  ↑ plasma or renal vein renin.


Thrombotic Microangiopathies

  • characterized by microangiopathic hemolytic anemia, throbocytopenia, renal failure, thrombotic lesions in capillaries and arterioles in tissue beds.
  • have schistocytes in blood smear.  normal coagulation profile, normal fibrin split products.
  • two main forms: HUS and TTP
  • two pathogenic triggers: endothelial injury, and platelet activation and aggregation.
    • endothelial injury ⇒ platelet activation and aggregation, thrombosis from ↓ PGI2 and NO production, ↑ endothelin ⇒ vasoconstriction.  adhesion molecules also recruit leukocytes which promote thrombosis.
    • platelet aggregation from ↑ large vWF from a deficiency of ADAMTS13 caused by Ab (common) or inherited (not common) ⇒ activate platelet spontaneously
  • tissue dysfunction from microthrombi, vascular obstruction, and tissue ischemia.


Typical Hemolytic-Uremic Syndrome (HUS)

  • aka epidemic, classic, diarrhea-positive.
  • follows infection with O157:H7 E. coli ⇒ Shiga-like toxin.  from ground hamburger, drinking water, raw milk, person-person transmission.
  • usually kids or elderly
  • prodrome = influenza-like or diarrheal symptoms.  then sudden onselt hematemesis and melena, severe oliguria, hematuria, associated with microangiopathic hemolytic anemia, thrombocytopenia, and prominent neurologic changes.  HTN in 50%.
  • Shiga-like toxin damages endothelium ⇒ ↑ leukocytes adhesion molecules, ↑ endothelin, ↓ NO, with TNF have endothelial apoptosis ⇒ platelet activation and vasoconstriction
  • schistocytes on blood smear, normal coagulation times, normal fibrin split products.
  • morphology: acute = patchy or diffuse cortical necrosis, thickened capillary walls, subendothelial deposits of fibrin and cell debris, fibrinoid necrosis of interlobular arteries and arterioles, occlusive thrombi
  • tx: dialysis


Clinical Case:

A 9 year old male presents to the ER with sudden onset bloody vomiting and bloody urine.  Mother states he had been feeling achey during the morning.  On presentation he is not very lucid.  Culture of the stool is positive for E. coli O157:H7.  Biopsy reveals microthrombi and thrombi in the kidney along with  capillary wall thickening.

What does this child have?

typical HUS


Atypical Hemolytic-Uremic Syndrome (HUS)

  • aka non-epidemic, diarrhea-negative.
  • in adults.
  • 50% have inherited deficiency of complement factors (ex. factor H). a few have mutated factor I or CD46
  • 50% have relapses and progress to end-stage renal disease.
  • associated conditions: antiphospholipid syndrome, pregnancy/postpartum, vascular diseases of kidney, chemo and immunosuppressive drugs, irradiation of kidney.
  • can have neurologic symptoms.  
  • have schistocytes on blood smear, normal coagulation times, and normal fibrin split products.
  • morphology: acute = patchy or diffuse cortical necrosis and subcapsular petechiae, glomeruli occluded by thrombi, capillary walls thickened, subendothelial deposits of cell debris and fibrin, interlobular arteries and arteriols have fibrinoid necrosis and occlusive thrombi.
    • chronic = varying degrees of scarring.
      • LM: glomerli hypercellular with thickened capillary walls with splitting 'tram-track' basement membrane, onion-skinning of arteries and arterioles
      • manifests as renal failure and HTN.


Thrombotic Thryombocytopenic Purpura (TTP)

  • ****pentad: fever, neurologic symptoms, microangiopathic hemolytic anemia, thrombocytopenia, and renal failure.
  • caused by Ab or genetic defects ⇒ functional deficits in ADAMTS13
    • most commonly by inhibitory autoantibodies.
  • present as adults <40yrs.
    • CNS involvement is dominant feature, renal present in 50%.
  • tx: exchange transfusions and immunosuppressive therapy
  • have schistocytes on blood smear, normal coagulation times, and normal fibrin split products.
  • morphology: acute = patchy or diffuse cortical necrosis and subcapsular petechiae, glomeruli occluded by thrombi, capillary walls thickened, subendothelial deposits of cell debris and fibrin, interlobular arteries and arteriols have fibrinoid necrosis and occlusive thrombi.
    • chronic = varying degrees of scarring.
      • LM: glomerli hypercellular with thickened capillary walls with splitting 'tram-track' basement membrane, onion-skinning of arteries and arterioles
      • manifests as renal failure and HTN.


Atherosclerotic Ischemic Renal Disease

  •  atherosclerotic unilateral renal artery stenosis ⇒ HTN
  • bilateral renal artery disease common cause of chronic ischemia with renal insufficiency in older adults
  • tx: surgical revascularization.


Atherembolic Renal Disease

  • embolization of atheromatous plaques from aorta or renal artery into intraparenchymal renal vessels in elderly patients with severe atherosclerosis.  
    • contain cholesterol crystals which you see as rhomboid clefts
  • usually of no consequence.  
  • in elderly with compromised renal function may ⇒ acute renal failure usually after abd surgery on atherosclerotic aneurysms.


Sickle-Cell Disease Nephropathy

  • seen with Sickle-Cell disease or trait.
  • presentation: hematuria and diminished concentrating ability (hyposthenuria), proteinuria.
  • from accelerated sickling in hypertonic hypoxic renal medulla.  hyperosmolarity dehydrates RBC and ↑ intracellular HbS concentrations.
  • have patchy papillary necrosis.


Diffuse Cortical Necrosis

  • usually after an obstetric emergency like abruptio placentae, septic shock, or extensive surgery.
  • bilateral and symmetric = fatal without supportive therapy.
  • morphology: massive ischemic necrosis limited to cortex.  looks like acute ischemic infarct.
    • glomerular and arteriolar microthrombi usually focal.
    • acute necroses of small arterioles and capillaries
    • lesions patchy with coagulative necrosis
    • hemorrhages into glomeruli with formation of fibrin plugs in glomerular capillaries.
  • sudden anuria, terminating rapidly in uremic death.


Renal Infarcts

  • has limited collateral circulation, is 'end-organ', and gets 1/4 CO.  
  • most are due to emboli from left atrium and ventricle after an MI.
    • less frequently from vegetative endocarditis, aortic aneurysm, aortic atherosclerosis.
  • morphology: infarcts in kidney are white.  After 24hrs are sharply demarcated, pale, yellow-white areas with small irregular foci of hemorrhagic discoloration.
    • ringed by zone of intense hyperemia.
    • wedge-shaped, apex points towards medulla.
    • undergo progressive fibrous scarring ⇒ V shaped depressed, pale, gray-white scars. undergo ischemic coagulative necrosis.
  • presentation: usually silent.  can have pain with tenderness at CVA with red cells in urine.


Agenesis of the Kidney

  • have bilateral agenesis in stillborn kids.
    • associated with limb defects and hypoplastic lungs ⇒ early death.
  • unilateral agenesis is uncommon.  can live as long as no other abnormalities.
    • opposite kidney enlarged from compensatory hypertrophy.
    • can develop glomerular sclerosis from adaptive changes in hypertrophied nephrons.



  • bilaterally ⇒ renal failure in early childhood.
  • unilateral = acquire scarring from vascular, infectious, or parenchymal diseases.
  • truly hypoplastic kidney has no scarring and has ↓ number renal lobes and pyramids (<6)
  • oligomeganephronia = small kidney with fewer nephrons that are hypertrophied.


Ectopic Kidney

  • lie just above pelvic brim or within the pelvis
  • normal or slightly small kidneys.  
  • kinking or tortuosity of ureters ⇒ obstruction to urinary flow ⇒ ↑ risk bacterial infections.