Four features of nephritic syndrome
1. Microscopic hematuria 2. HTN 3. Edema 4. Proteinuria
Four features of nephrotic syndrome
1. Proteinuria (> 3.5 g/24 hr) 2. Hypoalbuminemia 3. Edema 4. Hyperlipidemia **increased risk of infection, hypercoagulability
What are three primary glomerular disorders that typically cause nephrotic syndrome?
-Minimal change disease -Focal segmental glomerulosclerosis -Membranous glomerulonephritis (glomerulopathy)
What is the most common cause of nephrotic syndrome in adults? Second most common?
FSGS is most common. Membranous glomerulonephritis is 2nd.
Minimal change disease features
-Only finding on biopsy is podocyte effacement -Usually in kids and young adults -Treat with steroids (don't need to biopsy) -associated with NHL and Hodgkin's
FSGS is more common in what groups?
Black people, Hispanic people
HIV, obesity, heroin use
FSGS often presents with what?
HTN and hematuria in addition to nephrotic syndrome features
What are the primary and secondary causes of membranous glomerulopathy?
Primary: idopathic Secondary: Hep B, Hep C, malaria, drugs (e.g. gold), neoplasm (e.g. lung, colon, CLL), autoimmune d/o (e.g. SLE)
What are some causes of nephritic syndrome/hematuria?
-IgA nephropathy (Berger's) -Post-strep GN -Goodpasture's (anti-GBM) -Lupus nephritis -ANCA-associated -Membranoproliferative GN
What is the deal with IgA nephropathy?
Presents SHORTLY after a URI -most common cause of recurrent hematuria, but renal function is just fine in most patients
When does post-strep GN occur?
10-21 days after the strep URI or impetigo C3 will be decreased but C4 normal self limited course
Goodpasture's syndrome consists of
Proliferative GN, pulmonary hemorrhage, anti-GBM antibody. Treat with plasmapheresis, immunosuppression *linear deposits
What are the ANCA-associated causes of nephritis?
Granulomatosis with polyangiitis, polyarteritis nodosa
What are the causes of membranoproliferative GN?
Hep C, also Hep b, syphilis, lupus. Associated with cyroglobulinemia
What's the difference between MPGN and membranous GN?
Membranous is usu nephrotic, and deposits are subepithelial. MPGN is usually nephritis and deposits are subendothelial
Other important secondary glomerular diseases?
HTN nephropathy Diabetic nephropathy Lupus Sickle cell nephropathy Amlyoidosis HIV nephropathy
Proteinuria, edema, hematuria. Tx: prednisone, Ace-I and HAART. Hist resembles collapsing form of FSGS
Acute interstiital nephritis features
-recent infection or start of new med -may have fever, rash, eosinophilia, eosinophiluria -AKI
Acute vs. chronic interstitial nephritis
Acute: AKI with interstitial lymphs or eosinophils Chronic: indolent course assoc with tulointerstitial fibrosis and atrophy
What are the causes of renal papillary necrosis?
1. Analgesic nephropathy [may cause sterile [pyuria]
2. Sickle cell disease
3. UTI or urinary tract obstruction
4. Chronic alcoholism
5. Transplant rejection
Renal tubular acidosis (RTA) type 1
Type 1 (distal): cannot excrete H+ in distal tubule so cannot acidify urine --> hypokalemia, metabolic acidosis, renal stones, rickets in children
tx: sodium bicarb, phosphate salts
causes: lithium, amphotericin B, SLE, SCD, hepatitis
RTA type 2
Type 2 (proximal): cannot absorb bicarb in proximal tubule --> metabolic acidosis, hypokalemia
tx: Na restriction (increases proximal Na reabsorption and thus bicarb absorption)
causes: myeloma, Fanconi syndrome, amyloid, autoimmune
RTA1 and RTA2 both lead to what type of metabolic acidosis
Hypokalemic, hyperchloremic non-anion gap metabolic acidosis
RTA type 4
Type 4: Any condition assoc with hypoaldosteronism --> hyperkalemia, hyponatremia. Dec Na absorption + dec K and H excretion in distal tubule. Acidic urine in presence of metabolic acidosis.
causes: majority caused by diabetes. also- Addison's, sickle cell
Hematuria, HTN, palpable kidneys.
Tx: tx HTN and eventual transplant
Extra-renal manifestations: hepatic cysts (most common), intracranial aneurysm (do not screen), colonic diverticula, abdominal hernia, valvular heart dz
Liver involvement always present and may be the major feature. Pulmonary hypolasia 2/2 enlarged kidneys in utero, can cause Potter syndrome.
AR defect of amino acid transporter --> decreased intestinal and renal reabsorption of amino acids such as tryptophan --> nicotinamide deficiency
Hereditary or acquired proximal tubule dysfunction --> glucosuria, phosphaturia (leads to bone problems), proteinruia, polyuria, hpokalemia, type 2 RTA tx: supplement phos, alkali, salt, K, hydrate
Acute tubular necrosis causes
1. Ischemic AKI 2. Nephrotoxic AKI (e.g. abx, toxins, myoglobinuria, NSAIDs)
ATN urine microscopy
Muddy brown casts
Diabetic nephropathy pathology
GFR elevation --> basement membrane thickening --> mesangial expansion --> glomerulosclerosis.
Nodular glomerulosclerosis of pathognomic but diffuse is more common. Hyalinosis affecting BOTH afferent and efferent arterioles is also pathognomic.
Most common type of kidney stone?
Calcium oxalate (envelope shaped)
What is the pathophys of membranoproliferative GN type 2?
Type 2: dense deposit disease. Due to persistent activation of complement pathway
other types caused by immune complex deposititon
Renal cell carcinoma physical exam
Classic triad (not common): flank pain, hematuria, palpable flank mass
Left-sided varicocele that doesn't drain when recumbent
Paraneoplastic: anemia, thrombocytosis, hypercalcemia, cachexia
Dx: CT scan
What antibiotics are particularly nephrotoxic?
Aminoglycosides (e.g. gentamicin, amikicin, neomycin)
Methanol ingestion causes what symptom?
HIGH lactate levels, bitter almond taste
Antidote: sodium thiosulfate, hydroxocobalamin
What drugs can commonly cause hyperkalemia?
- Beta blockers
- Succinylcholine (NM blocker used in intubation)
What cause of nephrotic syndrome is most often assoc with renal vein thrombosis?
Membanous nephropathy, most often in association with adenocarcinoma
Waxy or broad casts = ?
Chronic renal failure
WBC casts = ?
Interstitial nephritis or pyelonephritis
Fatty casts = ?
Mutation in type IV collagen. Family history. Hematuria, basket weaving on electron microscopy.