Intrarenal diseases Flashcards by Maya Birchler

Due to uremia or underlying cause –
Decreased urine output, fluid retention, swelling in legs, ankles, feet

Daytime drowsiness
fatigue/weakness
Excessive thirst
N/V
SOB
Irregular heartbeat
Chest pain or pressure
Confusion

Severe = seizures or coma

acute tubular necrosis

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What puts someone at risk for acute tubular necrosis?

Recurrent kidney infection/recurrent nephritis
Kidney trauma (blunt/sharp injury)
Adverse reaction to transfusions
Prolonged HOTN and hypoxemia → poor circulation of blood in kidneys
Post-op phase of major surgery due to hypoperfusion
Complications following surgery

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Sudden damage or death of the renal tubule/epithelial cells of tubule → acute tubular necrosis → AKI
* MCC of intrinsic kidney disease from either ischemia or nephrotoxic exposure

acute tubular necrosis

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Ischemia
- Prolonged prerenal AKI (HOTN, hypovolemic, hypoxic, postop, sepsis)

Nephrotoxic exposure (exogenous, endogenous)
- Endogenous: myoglobinuria (rhabdo), Hgb, hyperuricemia, Bence-Jones
- Exogenous: AGs, amphotericin B (vanc, IV acyclovir, cephalosporins), radiologic contrast dye, calcineurin inhibitors (tacrolimus, cyclosporine)
→ destruction/apoptosis of cells → renal tubular/epithelial casts in urine (muddy brown casts)

acute tubular necrosis

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What are endogenous causes of acute tubular necrosis?

myoglobinuria (rhabdo), Hgb, hyperuricemia, Bence-Jones

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What are exogenous causes of acute tubular necrosis?

AGs, amphotericin B (vanc, IV acyclovir, cephalosporins), radiologic contrast dye, calcineurin inhibitors (tacrolimus, cyclosporine)

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elevated BUN + Cr with BUN/Cr <20:1
Hyperkalemia, hyperphosphatemia, hypocalcemia
ABG
UO: <500mL/24 hours or nonoliguric

Urinalysis: Na>40, FeNa>2%

Muddy brown casts (granular) or renal tubular epithelial cells

Low urine specific gravity (isosthenuria = inability to concentrate urine)

Low urine osmolarity

acute tubular necrosis

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What are the 3 phases of acute tubular necrosis?

Initial injury

Maintenance phase
- Oliguric (UOP<500) or nonoliguric
- Average duration 1-3 weeks
- Cellular repair + removal of debris
Recovery phase
- Diuresis
- GFR rising
- BUN+Cr falls

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How do you treat acute tubular necrosis?

Fluid therapy and monitoring I&Os, removing offending agent

Widespread use of diuretics should be avoided in critically ill
Nutritional support, kidney adjustment

Dialysis

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When is dialysis indicated in acute tubular necrosis?

Worsening acidosis
Life-threatening electrolyte disturbances
Worsening abnormalities or intoxication
Volume overload unresponsive to diuresis
Uremic complications
–> (AEIOU)
Acid-base
Electrolyte
Intoxications
Overload
Uremic sx

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AEIOU

Acid-base
Electrolyte
Intoxications
Overload
Uremic sx

dialysis!

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Triad of fever, maculopapular rash, and arthralgias

oliguria, peripheral blood eosinophilia

acute interstitial nephritis

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inflammatory/allergic response in interstitium of kidney in response to drugs, infections, autoimmune diseases, idiopathic
– NSAIDs, PCNs, sulfa, cephs, rifampin, cipro, allopurinol, diuretics, phenytoin, PPIs

acute interstitial nephritis

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Urinalysis: white cells, red cells, white cell casts, proteinuria (NSAID-induced)

Increased IgE, Cr, eosinophilia

Biopsy is gold standard

acute interstitial nephritis

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How do you treat acute interstitial nephritis?

Supportive → remove inciting agent + steroids

If symptoms continue, IV methylprednisolone and PO prednisone

Urgent dialysis occurs in up to ⅓ of all cases

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SMART NAC (nephrons are crying)

Sulfonamides
Methicillin
Ampicillin
Rifampicin
Thiazides
NSAIDs
Allopurinol
Cimetidine

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Cola colored/dark/smoky urine
Edema
HTN

Fever, abdominal/flank pain

AKI = oliguria with <500ml UO

HTN + azotemia + oliguria + hematuria (RBC casts) = hallmark

nephritic syndrome

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“Glomerulonephritis” - acute decrease in GFR leading to sodium retention

Inflammation → cytokine release → capillary damage → leakage of proteins and RBCs

nephritic syndrome

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Proteinuria <3/day
Hematuria → red cell casts, dysmorphic RBCs
Oliguria from lowered GFR (<400)
Azotemia from insufficient filtering + excretion of urea with increased BUN
Salt retention

Blood test: increased Cr, decreased GFR

Biopsy = hypercellular; (crescent-shape means rapidly progressive glomerulonephritis)

nephritic syndrome

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what can help categorize nephritic syndrome?

immune complex disease markers, ANCAs, anti-GBM antibodies, C3 glomerulopathy, monoclonal Ig mediated

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How do you treat nephritic syndrome?

Supportive - anti-HTN, steroid, cytotoxic agents, plasmapheresis
Edema, hypervolemia, HTN = BBs, CCBs, loop diuretics

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Onset 1-3 weeks after infection – scanty, cola-colored/dark urine, HTN

Type III hypersensitivity
commonly 2-14 year boy with facial periorbital edema up to 3 weeks after strep

Following group A strep infection, commonly pharyngitis or impetigo – deposition of immune complexes against organisms elicit acute inflammatory response

Also: staph, HIV, pneumonias, CMV, abscesses, mono, endocarditis, coccidiomycosis, shunt, malaria, hepatitis, syphilis, mycobacteria, toxoplasmosis

infection-related

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infection related is

a type of glomerulonephritis

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Immune complex –
Dx: increased antistreptolysin titer (ASO)
Biopsy = glomeruli appear enlarged + hypercellular
Immune complex depositions of IgG, IgM, C3 → “lumpy-bumpy appearance” → dome shaped subepithelial immune-complex deposit “humps”

infection-related glomerulonephritis

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How do you treat infection-related glomerulonephritis?

Post-strep AGN = supportive +/- abx

Developed within 1-2 days after URI gross/microscopic hematuria, URI, smoky-colored urine 1-2 days after illness Asia Children and young adults Males HIV, celiac, hepatic cirrhosis, CMV inheritable

IgA neuropathy glomerulonephritis

“Berger’s disease”- MC primary glomerular disease Immune complex – Dx: IgA may be increased Indication for renal biopsy: Proteinuria >500-1000 Elevated S creatinine New onset HTN or worsening Biopsy = mesangial IgA deposits + C3 deposits on immunofluorescence

IgA neuropathy glomerulonephritis

How do you treat IgA neuropathy?

Low risk = monitor High risk (proteinuria >1g/day, decreased GFR/HTN) = ACEI or ARB → SGLT2 inhibitors

Rash (palpable red-purple spots on buttocks, legs, feet) + abdominal pain + arthralgias/arthritis + renal issues GI: belly pain, nausea, vomiting, bloody stools Kidney: protein or blood in urine

IgA vasculitis (HSP)

2-6 Males Infections or medications “Henoch-schonlein purpura” – small vessel vasculitis associated with IgA deposition in vessel walls involving skin, joints, intestines, kidneys

IgA vasculitis (HSP)

Immune complex – LABS: decreased GFR< hematuria/proteinuria Biopsy = renal lesions → mesangial proliferation similar to IgA neuropathy

IgA vasculitis (HSP)

How do you treat IgA vasculitis?

Self limited, generally – rest, fluids, pain meds Steroids for persistent proteinuria Rituximab and plasma exchange for severe cases

Underlying lupus infection Nonwhites Deposition of circulating immune complexes

lupus glomerulonephritis

Immune complex – DS-DNA → biopsy to verify disease = “wire-looping” appearance of capillaries on light microscopy and granular appearance on immunofluorescence All patients with SLE should have routine urinalysis to monitor for hematuria or proteinuria Abnormal = biopsy

lupus glomerulonephritis

How do you treat lupus glomerulonephritis?

ACE or ARB Hydroxychloroquine → Steroids then cyclophosphamide or mycophenolate (blacks/hispanics/fertility/less SE)

Purpuric and necrotizing skin lesion in dependent lesions, arthralgias, fever, hepatosplenomegaly Underlying etiology = HCV infection causing vasculitis

cryoglobulin-associated glomerulonephritis

Immune complex – LABS: low complement, elevated Rh factor Kidney biopsy

cryoglobulin-associated glomerulonephritis

cryoglobulin-associated glomerulonephritis tx

Treat underlying infection – steroids, plasma exchange, rituximab

Fever, malaise, weight loss, present several months before other symptoms: Hematuria, proteinuria Vasculitic = purpura, mononeuritis Granulomatosis have upper or lower RT symptoms with nodular lesions Hemoptysis = concerning

pauci-immune glomerulonephritis

autoantibody vasculitis from ANCA Types: 1) microscopic polyangiitis 2) granulomatosis with polyangiitis 3) eosinophilic granulomatosis with polyangiitis

Pauci-immune glomerulonephritis

(small blood vessels, +P-ANCA) with kidneys, lungs, nerves, skin, joints NOT sinuses, NO granulomas

microscopic polyangiitis (pauci-immune glomerulonephritis)

(vasculitis and granulomas found in affected tissues with +C-ANCA) with sinuses, nose, trachea, lungs, kidneys, neuro (Wegener’s granulomatosis)

granulomatosis with polyangiitis (pauci-immune glomerulonephritis)

(in those with history of airway allergic hypersensitivity +P-ANCA and severe asthma, eosinophilia + systemic vasculitis with blood/tissue) - Churg-Strauss disease in heart, joints, lungs, nerves

Eosinophilic granulomatosis with polyangiitis (pauci-immune glomerulonephritis)

+ ANCA GN – LABS: serologic to determine ANCA Biopsy = necrotizing lesions and crescents on light microscopy Immunofluorescence = negative for immune complex deposition “pauci-immune”

pauci-immune glomerulonephritis

How do you treat pauci-immune glomerulonephritis

Induction = high dose steroids Immunosuppressive agents (cyclophosphamide, methotrexate, mycophenolate, rituximab) Plasma exchange Prophylaxis for jirovecii

URI → hemoptysis, dyspnea, respiratory failure, rapidly progressing URI in young adult males Pulmonary infections, smoking, hydrocarbon solvent exposure Antibodies attack the basement membrane in the kidneys Type II hypersensitivity

anti-glomerular basement membrane, "good pasture"

anti-GBM – CXR: pulmonary infiltrates if pulmonary hemorrhage is present anti-GBM antibodies Kidney biopsy = crescent formation with linear IgG staining along the GBM

anti-glomerular basement membrane, "good pasture"

How do you treat anti-glomerular basement membrane, "good pasture"?

High dose steroids + cyclophosphamide + plasmapheresis Refractory = rituximab

Glomerular injury resulting from deposition of immune complexes and/or complement mesangium along glomerular capillary walls Immune-complex mediated – commonly with viral hepatitis, autoimmune diseases Complement mediated Primary = idiopathic Secondary (MC) = autoimmune diseases (SLE), cancer, infections (HCV, HBV)

membranoproliferative glomerulonephritis

Monoclonal antibody immune complex – Diagnosis requires biopsy Light microscopy = diffuse mesangial cell proliferation w/ capillary wall thickening IF = determining if deposits are due to immune complexes Electron microscopy = determining location of deposits

membranoproliferative glomerulonephritis

how do you treat membranoproliferative glomerulonephritis?

Immune complex = supportive, otherwize consider steroids, immunosuppressives, cytotoxic agents, transplant C3 glomerulopathy = mycophenolate mofetil (MMF) + steroid → eculizumab → clinical trials → plasmapheresis

Wide variety and depends on nature and physicochemical properties of immunoglobulin Hematological condition where renal injury is occurring from MIg secretion that do not meet criteria for other therapies

monoclonal immunoglobulin glomerulonephritis

monoclonal immunoglobulin glomerulonephritis tx

Targeting plasma cell or B-cell clone in order to prevent renal deterioration, treating CKD, extrarenal manifestations

Within days, weeks, months with rapid progression to ESRD Nephritic syndrome presentation Older adults Rapid destruction of renal glomeruli All causes can cause this

rapidly progressiving glomerulonephritis

LABS: rapid rise in BUN + Cr Urine = hematuria, RBC casts, proteinuria Biopsy = crescent moon shaped deposits

rapidly progressiving glomerulonephritis

rapidly progressiving glomerulonephritis tx

Steroids + cyclophosphamide Goodpasture syndrome = + plasmapheresis ANCA-ass = same as above

Severe + generalized edema: periorbital (children), scrotal, ankles, feet Foamy urine Weight gain Dyspnea, transudative pleural effusion, DVTs HTN

nephrotic syndrome

Damage to the glomeruli and its filtration barrier selectivity → increased glomerular permeability → nonselective proteinuria → reactively increased hepatic function to compensate MCC: DM PRIMARY = diseases that only affect kidneys - Minimal change disease - Focal segmental glomerulosclerosis - Membranous nephropathy SECONDARY = extrinsic diseases - DM nephropathy - HIV-ass. Nephropathy - Renal amyloidosis

nephrotic syndrome

Proteinuria >3g/day - confirm with 24 hour urine collection or spot urine Hypoalbuminemia Hyperlipidemia - fatty casts in urine, lipiduria = “maltese cross” signs Hypercoagulable state Blood = low protein, increased cholesterol, TGs, ESR, low vitamins US = enlarged kidneys Confirm with biopsy = hypocellular

nephrotic syndrome

How do you treat nephrotic syndrome?

Treat underlying cause – diet control (restrict salt, fat, fluid) >10g/day = protein replacement HTN: ACEIs or ARBs Edema: diuretics Cholesterol: statins Anticoags: heparin, warfarin, dabigatran, rivaroxaban Immune system suppression: steroids for conditions that can cause this syndrome

Nephrotic symptoms MCC of nephrotic syndrome in children Idiopathic, following viral URI, hypersensitivity allergies, Hodgkin’s lymphoma, autoimmune, SLE, lithium, NSAIDs → structural deficit of podocyte → loss of negative electric charge

minimal change disease

Electron microscope = podocyte effacement/damage, fusion Proteinuria

minimal change disease

how do you treat minimal change disease?

Prednisone Refractory = cytotoxic therapy

Hematuria, HTN, proteinuria, renal insufficiency Focal and segmental become sclerotic/scarring → podocyte damage Primary – abnormalities, polymorphisms Secondary – HTN (AA), obesity, COVID, sickle cell, HIV, reflux neuropathy, analgesic, bisphosphonates)

focal segmental glomerulosclerosis

Kidney biopsy Damage to podocytes Light microscopy = segmental sclerosis and loss of podocytes IF = IgM + C3 seen in sclerotic lesions

focal segmental glomerulosclerosis

how do you treat focal segmental glomerulosclerosis?

Steroids 4-16 weeks Diuretics for edema ACE/ARB for proteinuria + HTN Statins SGLT-2 inhibitors Cytotoxic drugs Transplant Progresses to ERSD :(

Nephrotic-nephritic picture – Asymptomatic or: Edema, frothy urine Venous thrombosis may be first sign (have higher risk of hypercoagulable state) Underlying infection/neoplasm White, >40, male

membranous nephropathy

Nephrotic syndrome ass w/ thickened glomerular basement membrane from immune complex deposition MCC of primary nephrotic syndrome in adults Primary = idiopathic, PLA2R Secondary = SLE, infections (B/C, syphilis, endocarditis), drugs (PCN, NSAIDs, captopril), tumors

membranous nephropathy

PLA2R = diagnostic for primary nephropathy (don’t need biopsy) Kidney biopsy to confirm → thickened GBM with a spike and dome pattern

membranous nephropathy

how do you treat membranous nephropathy?

Treat underlying cause Treat for primary based on risk of renal disease progression → low risk: conservative – salt restriction, ACEI/ARBs for HTN, diuretics for edema, statins, anticoagulants → high risk: steroid + cyclophosphamide, cyclosporine, rituximab

More prone to other renal diseases including: AKI from IV contrast, concomitant use of ACE/ARB, NSAIDs Male AA + NA Family history MCC of ESRD in the US, MCC of secondary nephrotic syndrome Hyperfiltration injury → hypertrophy → sclerosis → podocyte injury → microalbuminuria → nephrotic syndrome

diabetic nephropathy

Diffuse glomerulosclerosis initially Nodular glomerulosclerosis with formation of Kimmelstiel-Wilson nodules = pathognomonic GFR declining over time, kidneys enlarged Biopsy not needed LABS: increased GFR, microalbuminuria

diabetic nephropathy

Aggressive → WL with obesity, strict glycemic control, control BP to <120/80 ACE/ARB with microalbuminuria + SGLT-2 inhibitors GLP-1 agonists treat/limit cardiac risk factors Renal transplant recommended for healthy with minimal comorbid conditions

diabetic nephropathy

More prone to other kidney diseases such as: Medication toxicity, vascular disease, diabetes, immune complex-mediated glomerular disease Nephrotic syndrome + declining GFR associated with low CD4 and AIDS

HIV-ass nephropathy

Biopsy = FSGS with glomerular collapse

HIV-ass nephropathy

how do you treat HIV-ass nephropathy?

Antiretroviral therapy for all patients with CKD or ESRD ACE/ARBs to control BP and slow disease progression Steroids Kidney transplant

Extensive proteinuria, enlargement of kidneys, rarely HTN, other organ enlargement

amyloidosis

Kidney = MC organ from tissue deposition of an abnormally folded protein Primary (MC) from plasma cell dyscrasia (overproduction of monoclonal Ig light chain) Secondary of chronic inflammatory disease such as RA, IBD, chronic, buildup of serum amyloid A protein

amyloidosis

LABS: proteinuria, decreased GFR – serum and urine protein electrophoresis tests - look for monoclonal spike → serum free light chains Polarized light = glomeruli are filled with amorphous deposits that show green birefringence with Congo red staining

amyloidosis

how do you treat amyloidosis?

Limited = steroids, chemotherapy agents

what are mixed nephrotic/nephritic syndromes?

membranous nephropathy membranoproliferative glomerulonephritis

nephritic syndromes

Infection related IgA neuropathy IGA vasculitis (HSP) Lupus glomerulonephritis Cryoglobulin-associated glomerulonephritis* Pauci-immune glomerulonephritis * Anti-glomerular basement membrane/good pasture Membranoproliferative glomerulonephritis* Monoclonal immunoglobulin glomerulonephritis

nephrotic syndromes

Minimal change disease Focal segmental glomerulosclerosis Membranous nephropathy Diabetic nephropathy HIV-associated nephropathy Amyloidosis

Intrarenal diseases Flashcards

(83 cards)