Renal Disease - GU Flashcards
Pre-renal vascular compromise
- 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
Renal Artery Stenosis
-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
Renal Artery Thrombosis
- 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
Renal Artery Aneurism
- Generally asymptomatic
- Hypertension present in 90 percent
- Dissecting aneurysms may cause flank pain and hematuria
Atheroembolic Renal Disease
-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
Renal Vein Thrombosis
- 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
Nephrotic Syndrome
- 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
Primary Nephrotic Syndrome
2/3
- Minimal-change nephropathy
- Focal glomerulosclerosis
- Membranous nephropathy
- Hereditary nephropathies
secondary Nephrotic Syndrome
1/3
- Diabetes mellitus
- Lupus erythematosus
- Amyloidosis and paraproteinemias
- Viral infections (eg, hepatitis B, hepatitis C, HIV)
- Preeclampsia
Presentation - Nephrotic Syndrome
Edema (serum albumin <3 g/dL)
- Dependent areas first, then generalized
- Periorbital
- Pulmonary edema, pleural effusions (dyspnea)
- Ascites (abdominal fullness)
-Infection, venous thrombosis
Labs - Nephrotic Syndrome
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
General Treatment - Nephrotic Syndrome
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
Minimal Change Disease - nephrotic syndrome
- 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
Membranous Nephropathy - Nephrotic Syndrome
- 5th-6th decade presentation usually
- Immune-mediated
- 50% progress to ESRD in 3-10 years
- Treatment is generally immunosuppressive
Focal Segmental Glomerulosclerosis - Nephrotic Syndrome
- 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
Diabetic Nephropathy - Nephrotic Syndrome
- 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
Acute Glomerulonephritis
-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
Acute Glomerulonephritis - Presentation
- 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
Acute Glomerulonephritis - Etiology
-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
Acute Glomerulonephritis - Epidemiology
- 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
Acute Glomerulonephritis - History
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
Acute Glomerulonephritis - Classic presentation and PE
- 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
Acute Glomerulonephritis -Labs
-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
IgA Nephropathy
-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