Glomerular Diseases Flashcards
Albumin
is the only measurable protein in urine on a urine dipstick. If have a positive urine dipstick for protein (albumin) you need to quantify with either a 24- hour urine collection or protein-creatinine / albumin-creatinine ratio on a random urine sample
Level of proteinuria is diagnostically helpful to distinguish tubulointerstitial disease vs glomerular disease
> 150mg/g- < 200mg/g = tubulointerstitial or glomerular disease
> 3500mg/g = glomerular disease
Albumin-creatinine ratio
measures albumin in urine
If positive and have retinopathy then diagnosis is diabetic nephropathy
30-300 mg/g “microalbuminuria”
> 300 mg/g = over proteinuria
Protein-creatinine ratio
is used to measure proteinuria
Proteinuria if a marker of renal parenchymal and glomerular disease and an independent predictor of progressive kidney disease, cardiovascular disease, and peripheral vascular disease
If you see proteinuria and hematuria on UA
suspect glomerular disease/injury
Molecule smaller than 3 nm can pass freely through the filtration membrane into the capsular space
Molecules includes:
Water
Electrolytes
Glucose
Amino acids
Nitrogenous wastes
Vitamins
Kidney infections and trauma commonly damaged the filtration membrane and allow protein (albumin) and blood cells to filter through
3 potential etiologies for Acute Kidney Injury
1-Pre-renal: low perfusion (60-70%)
Hypovolemia, hypotension
2-Post renal: obstruction to flow (5-10%)
BPH, urolithiasis, outlet obstruction
3-Intrarenal: intrinsic disease (25-40%)
1- Tubules ( Acute Tubular Necrosis)
2- Interstitium (Acute interstitial nephritis)
3-Glomerulus (Glomerulonephritis) RBC casts!!
Nephrotic Syndrome
General
Disease of the glomerulus, urinary excretion > 3.5 g protein in 24 hours
Hypoalbuminemia( < 3.0g/dL; nl 30g/L), hypercholesterolemia, edema and increase risk of thrombosis secondary to loss of protein S, C, and antithrombin III
Prognosis depends on cause and extent of renal damage
In USA most common cause is DM
Presentation
Urine: Albuminuria > 3.5g/day, “frothy”
Anasarca
Hypercholesteremia
Podocyte effacement on electron microscopy
Nephrotic Syndrome
primary vs secondary
Primary
results intrinsic process limited to kidney
Minimal change nephrotic syndrome (children post virus, tx w steroids)
Focal segmental glomerulosclerosis (black patients, HTN, heroin, HIV)
Membranous nephropathy (white patients, SLE, viral hepatitis, malaria)
IgA nephropathy
Secondary
systemic disease process with renal involvement
Diabetes ( yearly screen albuminuria)
Autoimmune Diseases
Systemic Lupus Erythematous
Amyloidosis
Sjogren syndrome
Sarcoidosis
Infection ( HIV, HCV,HBV)
Pre-eclampsia
Primary ( idiopathic) – glomerular injury is an intrinsic process limited to the kidney
Secondary – glomerular lesion is a result of a systemic disease with renal involvement
Nephrotic Syndrome
NAPHROTIC syndrome
Na + decrease
Albumin decrease
Proteinuria > 3.5 g/day
Hyperlipidemia
Renal vein thrombosis
Orbital edema
Thromboembolism
Infection (loss of immunoglobulins in urine)
Coagulopathy ( loss of antithrombin III, protein c/s in urine)
Nephrotic Syndrome
Work up
Urinalysis: proteinuria, lipiduria, glycosuria, hematuria, “foamy” urine
Microscopic examination of urine: RBC casts, granular casts, hyaline casts, fatty casts; oval fat body ( maltese cross)
BMP: low albumin ( < 2.5 g/dL), azotemia, hyperlipidemia, serum creatinine often normal
Renal biopsy
Collect a 24-hour urine to measure urinary protein: > 3.5 g of protein
Nephrotic Syndrome
Treatment
Rx: ACE-Inhibitors, loop diuretics to manage fluid overload; steroids ( work better in children); statins for hyperlipidemia
Education: Na and fluid restriction; no excessive protein/K intake, no NSAIDS
Strict blood pressure control: < 130/80 mmHg
Considerations: anticoagulation if thrombus present, if relapse or steroid non-responder may use cyclophosphamide, cyclosporine, or tacromilus
Pneumococcal vaccination
Nephrotic syndrome
Clin man / PE
Clinical Presentation:
Malaise, abdominal discomfort, anorexia, edema (face/scrotum) , oliguria, weight gain, shortness of breath, “frothy” urine
Physical Findings:
Skin stria, edema, retinal sheen, ascites, hypertension
Often mistaken for CHF
Primary Nephrotic Spectrum Diseases
Minimal Change Disease
Most common cause of proteinuric renal disease in children ( 80% of cases)
Causes
Primary
Idiopathic
Secondary
Following a viral upper respiratory infection
Associated with neoplasms ( leukemia/lymphoma)
Associated with hypersensitivity III reactions ( NSAIDs, Antibx, Bee stings)
Often resolves with a course of high-dose steroids ( 4 weeks)
Biopsy not always needed (renal biopsy would reveal nearly normal glomeruli- thus “ minimal change”
Primary Nephrotic Spectrum Diseases
Membranous Nephropathy
Most common cause of primary adult nephrotic syndrome
Causes
Primary (70% of cases)
Autoimmune process – IgG attacks phospholipase A2 receptor → podocyte injury
Secondary (30% of cases)
Associated with infections, malignancy, autoimmune disease, and certain drugs
50% of patients progress to ESRD over 3-10 years
Higher risk for hypercoagulable state than other forms of nephrosis
Particular predisposition for renal vein thrombosis
Secondary Nephrotic Spectrum Diseases
Diabetic Nephropathy
with tx
Most common cause of ESRD in the United States
More likely to develop in patients with type I diabetes
Develops ~10 years after the onset of diabetes
Progresses in stages
microalbuminuria → nephrotic proteinuria = decline in GFR
Treatment: strict glycemic control and ACEi
Glomerulonephritis AKA nephritic syndrome
acanthocytes
Dysmorphic RBC seen in glomerulonephritis
Proteinuria with dysmorphic RBC (acanthocytes) occurs because the RBC passes thru the glomerulus and is damaged- normal shaped RBC occurs when bleeding is from bladder or urethra
Glomerulonephritis
Common etiologies:
Glomerulonephritis
Poststreptococcal glomerulonephritis (PSGN)
IgA nephropathy (Berger’s disease) – most common cause worldwide
Wegener’s disease
Goodpasture syndrome (Anti-GBM antibody disease)
Lupus nephritis
Glomerulonephritis
Clin man
Presentation
Hematuria; “tea or coke colored urine”;
Hypertension
Oliguria or anuria
Edema of face and eyes in am- progressing to feet and ankles later in the day
Poststreptococcal glomerulonephritis (PSGN)
HAD STREP
Hypertension
ASO titer positive
Decreased GFR
Swelling
Tea-colored urine
Recent strep infection
Elevated BUN and Creatinine
Proteinuria
