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Renal Disease - GU Flashcards

1
Q

Pre-renal vascular compromise

A
  • Renal artery stenosis
  • Renal artery thrombosis
  • Renal artery aneurysm
  • Atheroembolic renal disease
  • Renal vein thrombosis
  • Generally associated with hypertension
  • Decreased blood flow to the kidney(s) as a result of renal vascular disease may cause an excessive amount of renin to be produced
  • Renin increases blood pressure
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2
Q

Renal Artery Stenosis

A

-Stenosis due to atherosclerosis in 80-90% or fibromuscular dysplasia

Clues

  • Sudden onset of hypertension < age 50 = fibromuscular dysplasia; > age 50 = atherosclerosis
  • Hypertension not responsive to three or more blood pressure medications
  • Increased urea
  • Unexplained kidney failure
  • Sudden kidney failure when first taking an ACE inhibitor
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3
Q

Renal Artery Thrombosis

A
  • Results from trauma, infection, aneurism, inflammatory disease or fibromuscular dysplasia
  • Acute complete blockage
  • Sudden onset of flank pain and tenderness
  • Fever, hematuria
  • Nausea and/or vomiting
  • Sudden decrease in kidney function
  • Hypertension
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4
Q

Renal Artery Aneurism

A
  • Generally asymptomatic
  • Hypertension present in 90 percent
  • Dissecting aneurysms may cause flank pain and hematuria
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5
Q

Atheroembolic Renal Disease

A

-Results from surgery, catheter insertion, anticoagulation

Clues

  • Skin lesions such as purpura, mottling of the toes and feet
  • Kidney failure, acute or chronic
  • Abdominal pain, diarrhea
  • Confusion, weight loss, fever, muscle aches
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6
Q

Renal Vein Thrombosis

A
  • Results from trauma, compression of a renal vein by an adjacent structure such as a tumor or aneurysm, nephrotic syndrome, pregnancy, steroid use, and OCPs
  • Chronic onset most often asymptomatic
  • Acute onset
  • Persistent severe flank that may be spasmodic at times
  • CVA tenderness
  • Decreased kidney function
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7
Q

Nephrotic Syndrome

A
  • A Glomerular problem of leaking protein
  • Proteinuria > 3 or 3.5 g/day
  • Hypoalbuminemia
  • Edema
  • Hyperlipidema
  • Oval fat bodies in the urine

Loss of protein in urine leads to
-Hypoalbuminemia, which causes -> Decreased plasma oncotic pressure, which ->Reduces ECV, thus circulating volume is decreased, so the kidney -> Increases Na and Water reabsorption in the tubules, which leads to -> EDEMA

Loss of protein in urine means:

  • Some of those proteins are endogenous immunoglobulins, which leaves the patient prone to: INFECTION
  • Some of those proteins are endogenous anticoagulants, which means: Hypercoagulable state, thus - ARTERIAL AND VENOUS THROMBOSIS

-Both hypoalbuminemia and diminished plasma oncotic pressure play a role in ->Increased hepatic production of VLDL, which results in -> HYPERLIPIDEMIA

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8
Q

Primary Nephrotic Syndrome

A

2/3

  • Minimal-change nephropathy
  • Focal glomerulosclerosis
  • Membranous nephropathy
  • Hereditary nephropathies
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9
Q

secondary Nephrotic Syndrome

A

1/3

  • Diabetes mellitus
  • Lupus erythematosus
  • Amyloidosis and paraproteinemias
  • Viral infections (eg, hepatitis B, hepatitis C, HIV)
  • Preeclampsia
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10
Q

Presentation - Nephrotic Syndrome

A

Edema (serum albumin <3 g/dL)

  • Dependent areas first, then generalized
  • Periorbital
  • Pulmonary edema, pleural effusions (dyspnea)
  • Ascites (abdominal fullness)

-Infection, venous thrombosis

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11
Q

Labs - Nephrotic Syndrome

A

UA - 24hr or UPCR
-Proteinuria due to effacement of podocytes and basement membrane damage - causes foamy urine

Blood has:

  • Hypoalbuminemia (<6 g/dL)
  • Hyperlipidemia (50% early)
  • Hypertrigliceridemia
  • Elevated ESR, low Vit D, zinc, and copper in some

Generally need Renal Biopsy for specific diagnosis

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12
Q

General Treatment - Nephrotic Syndrome

A

Protein Loss

  • Dietary protein to replace losses (protein restriction questionable)
  • ACE inhibitor or ARB to decrease intraglomerluar pressure [monitor serum Cr and K]

Edema
-Salt restriction + diuretics (thiazide and loop, often high doses)

Hyperlipidemia
-Dietary and pharmacologic

Hypercoagulable state
-If albumin <2 g/dL, anticoagulation therapy

REFER ALL TO NEPHROLOGY

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13
Q

Minimal Change Disease - nephrotic syndrome

A
  • most common in children
  • No change on biopsy under light microscopy, but podocyte effacement on electron microscopy
  • Idiopathic or post-URI, tumor, drugs, or hypersensitivity
  • Usually presents full-blown nephrotic
  • Rarely causes acute kidney injury
  • Treatment: Prednisone - continue for several weeks after resolution of proteinuria
  • Steroid-resistant nephrotic syndrome (4 weeks and persistent proteinuria) or relapses may need alternate treatment
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14
Q

Membranous Nephropathy - Nephrotic Syndrome

A
  • 5th-6th decade presentation usually
  • Immune-mediated
  • 50% progress to ESRD in 3-10 years
  • Treatment is generally immunosuppressive
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15
Q

Focal Segmental Glomerulosclerosis - Nephrotic Syndrome

A
  • Idiopathic or secondary to heroin use, morbid obesity, HIV, or chronic urinary reflux
  • Decreased renal function common at presentation
  • Progress to ESRD in 6-8 years
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16
Q

Diabetic Nephropathy - Nephrotic Syndrome

A
  • Most common cause of Glomerular disease and ESRD in the US (4000/yr)
  • Type I 30-40%, Type II 15-20% after 20 years
  • Males, Af Am, Nat Am higher risk
  • Albuminuria (macro or microscopic) precedes decline in GFR

Progression

  • Hyperfiltration (increase GFR)
  • Microalbuminuria (30-300 mg/d)
  • Albuminuria (>300 mg/dL)
  • GFR returns to normal, then decreases

Treatment - begin early

  • Aggressive glycemic control
  • Treatment of hypertension : Goal 125-130/75-80
  • ACE or ARBs slow progression
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17
Q

Acute Glomerulonephritis

A

-Immune-triggered inflammatory damage to the glomerulus

Nephritic Pattern
-Urine RBCs: Some dysmorphic and some acanthocytes which are diagnostic of glomerular hematuria if >= 5% of urinary RBCs
-Occasionally WBCs
\+/- Red cell or mixed cellular casts
-Variable proteinuria
18
Q

Acute Glomerulonephritis - Presentation

A
  • Sudden onset of hematuria, proteinuria, and red blood cell (RBC) casts
  • Often accompanied be hypertension, edema, azotemia (decreased GFR), and renal salt and water retention
  • Primary renal disease or secondary to systemic disease
  • Immune complexes deposited in or formed in the glomerulus
  • Enlarged glomeruli with infiltrating PMNs and Monocytes
  • Granular deposits of IgG, IgM, and C3 along GBM
  • Kidneys may be enlarged up to 50%

Most common presentation
-Acute facial puffiness with dark, scanty urine
Nonspecific symptoms
-Weakness, fever, abdominal pain and malaise

19
Q

Acute Glomerulonephritis - Etiology

A

-Infectious - Post-streptococcal (PSGN) or other

Non-infectious

  • Primary Renal - MPGN, Berger (IgA Nephropathy), etc.
  • Systemic Diseases - Vasculitis, SLE, PAN, HSP, Goodpasture
  • Other - Guillain-Barre, DPT vaccine, serum sickness
20
Q

Acute Glomerulonephritis - Epidemiology

A
  • Ig A Nephropathy most common worldwide
  • PSGN most common in children, incidence falling in Western countries
  • Males affected more often 2:1
  • No ethnic predominance
  • Some (post-infectious) socioeconomic variance
21
Q

Acute Glomerulonephritis - History

A

Onset

  • Usually abrupt
  • Post-infections up to 3 weeks, variable
  • PSGN - 1-2 weeks post pharyngitis or 2-4 weeks dermal
  • If only 1-4 days post-streptococcal – preexisting renal disease

SXS

  • Hematuria - Universal, even if microscopic
  • Gross hematuria (30% of pediatric patients) smoky-, coffee-, or cola-colored urine
  • Oliguria
  • Edema - mild (involving only the face) to severe, bordering on a nephrotic appearance
  • Headache - secondary to hypertension
  • Shortness of breath or dyspnea on exertion - This may occur secondary to heart failure or pulmonary edema - uncommon
  • Possible flank pain secondary to stretching of the renal capsule
  • Identify possible etiologic agent
  • Streptococcal throat infection or skin infection
  • Recent fever, sore throat, joint pains, hepatitis, travel, valve replacement, and/or intravenous drug use
  • Assess disease process symptoms
  • Loss of appetite, generalized itching, tiredness, listlessness, nausea, easy bruising, nosebleeds, facial swelling, leg edema, and shortness of breath
22
Q

Acute Glomerulonephritis - Classic presentation and PE

A
  • Triad of sinusitis, pulmonary infiltrates, and nephritis- Wegener granulomatosis
  • Nausea and vomiting, abdominal pain, and purpura - Henoch-Schönlein purpura
  • Arthralgias - SLE
  • Hemoptysis - Goodpasture syndrome or idiopathic progressive glomerulonephritis
  • May have normal exam and blood pressure, but most often edema and hypertension (75%)
  • Look for fluid overload signs
  • Periorbital and/or pedal edema
  • Crackles
  • Elevated jugular venous pressure
  • Ascites and pleural effusion
  • Also look for: Rash (vasculitis, HSP, or lupus nephritis), Pallor, CVA fullness or tenderness, Abnormal neurologic examination or altered level of consciousness (from malignant hypertension), Arthritis
23
Q

Acute Glomerulonephritis -Labs

A

-UA - look for dark urine, high specific gravity, protein, blood, dysmorphic RBCs, WBCs, RBC Casts

Blood Tests

  • Complete blood count (CBC)
  • Blood urea nitrogen (BUN), serum creatinine, and serum electrolytes (especially serum potassium)
  • Erythrocyte sedimentation rate (ESR)
  • Complement levels (C3, C4, CH50)
  • Renal US can be helpful to assess size (smaller kidneys are less likely to recover) and r/o obstruction
  • Renal Biopsy is not necessary to diagnose PSGN, but helps to guide therapy and prognosis; required for primary renal disease
24
Q

IgA Nephropathy

A

-Any age, peak 2nd and 3rd decade
-40-50% present with visible hematuria after URI
+/- flank pain and fever, mimics UTI or urolithiasis
-Recurrences over a few years
-30-40% present with microscopic hematuria and mild proteinuria noted incidentally - 25% will go on to gross hematuria
<10% present with nephrotic syndrome or edema/hypertension/oliguria with hematuria
-Associations - Cirrhosis, Celiac, HIV, AD Familial
-Diagnosis - Renal Biopsy: Generally not done unless more severe signs
-Acute kidney injury rare from tubular injury due to occulsion from hematuria

25
Q

IgA Nephropathy - Management

A
  • Patients with isolated hematuria, no or minimal proteinuria, normal GFR
  • No treatment, monitor every 6-12 mo
  • Patients with persistent proteinuria (above 500 - 1 g/day), normal or sl reduced GFR, mild to moderate histologic findings on renal biopsy
  • ACE inhibitor or ARB
  • Fish oil (3.3 grams/day or more) if protein excretion above 1 g/day despite three to six months of therapy with an ACE inhibitor or ARB
  • More severe disease: Anti-inflammatory/immunosuppressive therapy
  • Refer all patient with suspected IgA Nephropathy to a Nephrologist
  • Usually benign course but ESRD occurs in 15-20% of patients within 10 years of onset and in about 25-30% of patients by 20 years (biopsied patients only)
26
Q

Post-Streptococcal Glomerulonephritis (PSGN)

A
  • Typically age 2-12; 5% < 2; 10% >40
  • Disease severity and mortality much higher in adults
  • Presentation - Latent period after strep infection, dark urine, abrupt onset of periorbital edema
  • Nonspecific sx - anorexia, malaise, weakness, nausea and vomiting possible
  • HTN 60-80%; Oliguria 10-50% (transient); LV Dysfunction possible

Work up

  • As previously discussed, plus streptozyme
  • Will have elevated BUN and Cr, transient
  • Low serum complement
  • Proteinuria may be mild or full-blown nephrotic
27
Q

PSGN - Management

A
  • Symptomatic - control edema and blood pressure
  • Limit salt and water
  • Diuretics if severe edema or hypertension (Loop diuretics)
  • CCB or ACE for refractory HTN
  • Dialysis if life-threatening hyperkalemia, clinical uremia
  • Restrict activity until feeling well
  • Steroids not indicated
  • Treat family members for strep (throat culture everyone) with PenG or Erythromycin 7-10 days
28
Q

Hydronephrosis

A
  • An obstructive problem that may CAUSE tubulointerstitial disease
  • Hydronephrosis - distention of the renal calyces and pelvis with urine as a result of obstruction of the outflow of urine distal to the renal pelvis
  • Hydroureter is dilation of the ureter
  • May be physiologic or pathologic
  • Chronic or acute, bilateral or unilateral
29
Q

Hydronephrosis - Causes

A
  • Anatomic abnormalities - majority of pediatric cases
  • Urethral valves or stricture, or stenosis at the ureterovesical or ureteropelvic junction
  • Calculi - most common in young adults
  • Prostatic hypertrophy or carcinoma, retroperitoneal or pelvic neoplasms, and calculi - primary causes in older patients
  • Pregnant women - 80%, R>L, second trimester, persists 6-12 weeks postpartum
  • Increased ureteral pressure leads to -> Decline in GFR within hours which persists for weeks after relief of obstruction
  • Severe impairment of renal tubular ability to -> Transport sodium, potassium, and protons and Concentrate and dilute the urine
  • Brief disruptions - reversible functional disturbance
  • Chronic disruptions - profound tubular atrophy and permanent nephron loss
30
Q

Hydronephrosis - History

A

-Acute - Pain - distention of bladder, collecting system, or renal capsule
Stone or fluid load exceeding flow rate
-Non-acute - pain minimal or absent
Congenital UPJ obstruction or tumor

  • Upper - flank pain; Lower - pain radiates to ipsilateral testicle or labia
  • Anuria possible

Flags

  • Blood - stone
  • Fever or diabetes - urgent
  • Solitary kidney - emergent
31
Q

Hydronephrosis - Exam, labs, Tx

A
  • Kidney may be palpable
  • Bilateral hydronephrosis - LE edema common
  • CVA tenderness common
  • Distended bladder - Lower obstruction
  • Digital rectal exam for prostate hypertrophy, masses, etc.
  • UA ->Pyuria - infection, Microscopic hematuria - stone or tumor
  • CBC - check for leukocytosis/acute infection.
  • Chemistries -> Elevated BUN and creatinine, and hyperkalemia all possible

tx

  • Directed at relieving the obstruction
  • Generally surgical
32
Q

Polycystic Kidney Disease

A
  • A genetic architectural problem
  • Cystic enlargement of BOTH kidneys
  • Hypertension
  • Hematuria, polyuria
  • Flank pain
  • Recurrent UTIs
  • Heart valve defects (MVP) with infective endocarditis
  • Cerebral and aortic aneurysms
  • Liver cysts (with impaired function)
  • Renal Stones
  • Increased risk for renal carcinomas (ALL renal failure patients have a generally elevated cancer risk)
33
Q

PKD Genetics

A
  • Most forms of PKD are hereditary
  • AD (Autosomal dominant) most common
  • AR (Autosomal recessive)
  • Congenital PKD: 7.4% of dialysis and 9.5% of transplant patients
  • “Acquired” PKD - from aging, dialysis, drugs, hormones
34
Q

Autosomal recessive - PKD

A

-RARE - 1:20,000 live births
Morphology
-Elongation of renal collecting tubules into multiple cysts
-Often linked with fetal or neonatal death - enlarged kidneys + lung dysgenesis/pulmonary hypoplasia

35
Q

Autosomal dominant - PKD

A
  • Dominant Mendelian trait 1:800 live births
  • about 50,000 cases in US
  • MOST COMMON lethal condition inherited as a dominant trait!
  • Incomplete penetrance – highly variable expression pattern
  • Symptoms usually present in 3rd-4th decade (though cysts present prior to birth)
  • Pain is most common presenting symptom
  • Ultrasound is imaging of choice
  • Management is control of HTN, UTIs, hematuria, and pain
  • ESRD - Dialysis and Transplant
36
Q

Autosomal dominant - PKD - Risk factors

A
  • PKD1 genotype
  • Large kidneys
  • Several episodes of gross hematuria
  • Severe and frequent kidney infections
  • Hypertension
  • Multiple pregnancies
  • Black racial background
  • Male sex
37
Q

AD PKD History

A

Pain is most common - abdomen, flank, or back - from:

  • Enlargement of one or more cysts
  • Bleeding into cyst or ruptured w/ gross hematuria
  • Urinary tract infection (eg, pyelonephritis, infected cysts, perinephric abscess)
  • Nephrolithiasis and renal colic

OR pain may be from an associated condition

Hematuria : Self-limited, lasting 1 week or less

  • Polycystic kidneys are prone to injury: 60% have hemorrhages
  • Mild trauma - intrarenal hemorrhage or bleeding into the retroperitoneal space (PAIN!)
38
Q

AD PKD Exam

A

Hypertension (diastolic) - 50-75% of patients, even w/normal renal function

  • More severe early
  • Improves as the renal insufficiency progresses
  • Palpable, bilateral flank masses occur in patients with advanced ADPKD
  • Nodular hepatomegaly occurs in those with severe polycystic liver disease
39
Q

AD PKD Complications

A
  • End-stage renal disease (ESRD) - frequent
  • Polycystic liver disease
  • Cysts in liver, pancreas, spleen
  • Pain and infection
  • Cerebral aneurisms - 4-10%
  • Nephrolithiasis - 20-30%, uric acid stones more likely
40
Q

AD PKD Work up

A 
Who to work up
-Family history of PKD
-Hypertension + 
Recurrent UTIs (>2/yr)
Gross hematuria and/or polyuria
  • Ultrasound (also for screening relatives
  • Serum chemistry profile, including calcium and phosphorus
  • Complete blood cell count
  • Urinalysis
  • Urine culture
  • Uric acid determination
  • Intact parathyroid hormone assay
41
Q

AD PKD Treatment

A
  • Control blood pressure
  • Control abnormalities related to renal failure
  • Treat urinary tract infections
  • Treat hematuria
  • Reduce abdominal pain produced by enlarged kidneys (analgesics, cyst decompression)
  • Heart murmurs: AHA antibiotic prophylaxis
  • Refer to Nephrology for most up to date management
  • Monitor for and treat hyperkalemia, hyperphosphatemia, hypocalcemia, hyperparathyroidism, metabolic acidosis
  • Diet and Activity: Low salt if HTN or renal failure, NO CONTACT SPORTS

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