Nephrology Flashcards
Calcium receptor agonist used for secondary hyperparathyroidism
Cinacalcet
Hypercalcemia of malignancy not responding to bisphosphonate
Denosumab
Morphine toxicity: signs
nausea, pruritus, somnolence, delirium, myoclonus
High clinical suspicion of drug induced AIN: Mx
- No further testing
- Discontinue drug
PSGN begins _ to _ days after pharyngitis
PSGN begins 10 to 14 days after pharyngitis
Normal albumin: creatinine ratio
MustKnow: Attending
CK: Intern
< 30
Fixable risk factors for diabetic nephropathy
Hypertension, hyperglycemia
Urine osmolality in polydipsia
< 100
BUN Creatinine ratio in volume depletion
> 20
In normal and uncomplicated renal disease: ~10:1.
BUN:Cr > 20:1 in hypovolemia because of the increase in urea reabsorption.
- ~ 40 to 50 percent of filtered urea is reabsorbed, most in the PCT, where it is passively linked to the reabsorption of Na and H20.
- Increase in proximal Na reabsorption in hypovolemia produces a parallel increase in urea reabsorption.
- Net effect is a fall in urea excretion and elevations in the BUN and the BUN/serum creatinine ratio, frequently to greater than 20:1.
- This selective rise in the BUN is called prerenal azotemia.
- The serum creatinine concentration will increase in this setting only if the degree of hypovolemia is severe enough to lower the GFR.
Hyaline cast: imply
Concentrated urine, diuretics, non-specific
Hyaline casts — Hyaline casts are only slightly more refractile than water and have a transparent, empty appearance.
Hyaline casts may be observed with small volumes of concentrated urine or with diuretic therapy and are generally nonspecific.
Frequency of the full triad of features (fever, rash, eosinophilia)
< 10%
PSGN features
- Hypertension
- Edema
- Hematuria
- Proteinuria
- Hypocomplementemia
- 2-3 weeks after infection
IgA nephropathy vs PSGN
PSGN: 2-3 weeks after infxn, IgA: concurrent, within 2-3 days
Alport syndrome
- Mutations in type IV collagen
- Typically X-linked dominant
- Progressive glomerular disease to ESRD
- Ocular abnormalities (eg, anterior lenticonus),
- sensorineural hearing loss
Alport syndrome: why glomerular disease/
Mutations in Type IV collagen which is an important component of GBM
Contrast nephropathy prophylaxis: IVF
NS for 7 hours
EKG abnormalities in hypokalemia and hypomagnesemia
- Hypokalemia: U waves, T-wave flattening
- Hypomag: QT prolongation
Cocaine intoxication: eye finding
Mydriasis
Cocaine intoxication: why is dialysis useless?
Cocaine is 90% protein bound
Ethylene glycol and methanol poisoning: Rx
Fomepizole
Profound metabolic acidosis
Methanol or ethylne glycol poisoning
Few conditions other than methanol and ethylene glycol intoxication present with a profound metabolic acidosis (serum bicarbonate less than 8 meq/L), and most of these conditions present in a characteristic fashion (eg, status epilepticus, profound shock, ischemic bowel) .
Serum HCO3 < 8: Signifies
Ethylene glycol or methanol poisoning
Few conditions other than methanol and ethylene glycol intoxication present with a profound metabolic acidosis (serum bicarbonate less than 8 meq/L), and most of these conditions present in a characteristic fashion (
- eg, status epilepticus,
- profound shock,
- ischemic bowel
CK greater than _ _ the normal limit is diagnostic of rhabdomyolysis
CK greater than 5 times the normal limit is diagnostic of rhabdomyolysis
AKI caused by rhabdo: CK is usually > 5K, often > 10K
Incontinence following radical prostatectomy: Rx1
Kegel
Tolteredine, oxybutinin: SideFx
Dry mouth, constipation, Drowsiness
Both anti-muscaranic agents, hence above SideFx
Oval fat bodies: why are they seen in nephrotic syndrome?
- There is heavy proteinuria (3.5 g/day).
- Lipoproteins are re-absorbed in the PCT.
- These PCT cells are desquamated.
- These are the oval fat bodies or lipid containing granular casts.
Muddy brown casts: Signify
ATN
Red urine: causes
- Beeturia
- Hemoglobinuria
- Myoglobinuria
- Hematuria
Grainy urine
Urolithiasis
Renal hemodynamic response to volume depletion
- Afferent arteriole: vasodilates by prostaglandin activity.
- Efferent arteriole: constricts due to angiotensin II
Hemolytic anemia, ARF, thrombocytopenia
HUS
Minimal change disease: presentation
Nephrotic syndrome
Nephrotic syndrome edema: RxStrategy
- Treat underlying condition
- Loop diuretic
Spironolactone is the only diuretic which decreases proteinuria but can cause hyperkalemia.
Hypocomplementemic glomerulonephritis: signifies
Post-infectious glomerulonephritis
PSGN vs Post-infectious GN
Same thing
PSGN: aetiopathogenesis
glomerular immune complex disease induced by nephritogenic strains of group A beta-hemolytic streptococcus (GAS)
PSGN: which complement is down?
C3
C4 is normal or mildly decreased
Streptozyme test: sensitivy/specificity
95% for Strep pharyngitis, 80% for cellulitis
Normal complement levels in autoimmune renal disease
- ANCA associated
- anti-GBM, Goodpasture
- IgA nephropathy
CKD IV + metabolic acidosis: what will slow progression?
Sodium bicarbonate
Target HCO3 > 22
Benefits:
- Slows decline
- Improves nutritional status
- Improves metabolic bone disease by limiting bone buffering.
Bone buffering
40% of the buffering of an acute acid load takes place in bone
An acid load leads to uptake of excess H+ ions by bone in exchange for surface Na+ and K+ and by the dissolution of bone mineral, resulting in the release of buffer compounds, such as NaHCO3, CaHCO3, and CaHPO4.
It has been estimated that at least 40% of the buffering of an acute acid load takes place in bone. Chronic acidosis can lead to: rickets, osteomalacia and osteopenia.
Rationale for using sevalemer
Non-calcium based; theoretical benefit, no evidence
Hyperphosphataemia in patients with chronic renal failure has traditionally been treated with calcium- and aluminium-containing phosphate binders. Sevelamer is a novel non-calcium-, non-aluminium-containing phosphate binder.
Phosphate binders: why are they used in CKD?
Correct hyperphosphatemia
- Decreased renal excretion of phosphate causes:
- Secondary hyperparathyroidism which causes
- Soft tissue calcification, particularly arteries.
- HD only partially corrects hyperphosphatemia.
Hyperphosphatemia almost invariable in patients with end-stage renal failure. It is only partially corrected by intermittent haemodialysis; the majority of patients on this treatment have plasma phosphate levels above the normal range of 0.7– 1.5 mmol/l at the start of each dialysis, with more than a third over the recommended upper limit of 1.8 mmol/l [1] . This persistent hyperphosphataemia commonly leads to secondary hyperparathyroidism and soft-tissue calcification, which particularly affects the media and intima of the arterial tree. Arterial walls become more rigid, and pulse-wave velocity increases, leading to increased atherosclerosis of the coronary arteries and premature heart disease, which is the major cause of death in patients on long-term haemodialysis [2–6] . Chronic haemodialysis programs for end-stage renal failure have expanded to such an extent [7, 8]that there are now over a million patients on haemodialysis worldwide who are at risk of these complications, which also affect many patients with chronic renal failure who are not on HD.
Kidney stone type after Roux-en-Y bypass
Calcium oxalate
After a 6 week course of ciprofloxacin for pelvic discomfort, sense of incomplete emptying of the bladder, mild dysuria, the next step is:
Tamsulosin
Trial of α-adrenergic blocker
Urinary residual volume
< 100 ml
Recurrent UTI + high PRV in a man: Mx
TURP
Goserelin
Synthetic analogue of LHRH
Indixn: Prostate Cancer
5-α-reductase inhibitor: Indixn
- Cannot tolerate alpha-1-adrenergic antagonists
- do not have predominately irritant symptoms or
- erectile dysfunction
- Treatment for 6 to 12 months is needed to improve symptoms.
Finasteride and dutasteride: similar efficacy, similar adverse effects.
Normal serum calcium, recurrent renal stones, hypercalciuria: Mx
Thiazide diuretic
Why is serum ferritin level an underestimate of iron stores in CKD?
Tends to be elevated (acute phase reactant)
Divide measured level by 3 to get the right level
CKD: ferritin and transferrin saturations indicating Fe defn
- Ferritin < 500
- Transferrin sat < 30%
Serum iron: why is it not a definitive test of iron status?
Serum iron fluctuates with:
- dietary intake
- normal diurnal variation.
Serum iron is low in iron deficiency as well as in ACD. This is because levels of serum iron depend on the efficiency of iron recycling by bone marrow and reticuloendothelial macrophages, which is reduced in both conditions.
LR+ of ferritin <15 for Fe defn
52
A ferritin level ≤15 ng/mL had a likelihood ratio of 52-fold for iron deficiency
Ferritin levels in the range of 15 to 25: LR+ == 9
and 25 to 35 ng/mL: LR+==3
Serum transferrin
- Transferrin is a circulating transport protein for iron.
- Iron defn: increased in iron deficiency
- ACD: can be decreased in ACD.
Transferrin can also be reported as TIBC. The transferrin concentration (in mg/dL) can be converted to the TIBC (in mcg/dL) by multiplying by 1.389
TIBC and Transferrin saturation
- TIBC = k*transferrin_concentration
- The transferrin concentration (in mg/dL) can be converted to the TIBC (in mcg/dL) by multiplying by 1.389
- Transferrin saturation == (serum iron ÷ TIBC x 100).
- In iron deficiency, iron is reduced and TIBC is increased, resulting in a lower transferrin saturation.
- Transferrin saturation normal: 25 to 45 percent.
- Transerrin saturation < 10 common in individuals with iron deficiency, and a cutoff of below 16 percent is generally used to screen for iron deficiency, although other thresholds may be used in some settings such as pregnancy
Iron defn: increased in iron deficiency
ACD: can be decreased in ACD.
Transferrin saturation: why is it low in Fe defn?
- TIBC = k*transferrin_concentration
- Transferrin_saturation = (serum_iron/TIBC)*100
- TIBC goes up in Fe defn, serum iron goes down.
- Therefore transferrin saturation goes up
Unclear why transferrin goes up in iron defn anemia.
Serum transferrin – Transferrin is a circulating transport protein for iron. It is increased in iron deficiency but can be decreased in ACD. Transferrin can also be reported as TIBC. The transferrin concentration (in mg/dL) can be converted to the TIBC (in mcg/dL) by multiplying by 1.389.
FMD: +resistant hypertension
Rx
Renal artery PTCA
Renal-Sarcoid: +nephrocalcinosis + worsening renal failure: Rx
Increase dose of prednisone
Hypokalemia: Eating disorder + normal acid-base status
Why is this laxative abuse?
Diuretic abuse will cause alkalosis
Alkalosis: Contraction-alkalosis: Mechanism
Loss of sodium chloride rich fluids
- Setting: Loss of large volumes of fluid that has a high sodium chloride concentration but a low bicarbonate concentration.
- The bicarbonate concentration rises because there is contraction of the extracellular volume around a constant quantity of extracellular bicarbonate (and the chloride concentration simultaneously falls).
- This is offset by the release of hydrogen ions from cell buffers, which acts to stabilize the bicarbonate concentration.
Eg: IV loop diuretics to induce rapid fluid removal often causes a metabolic alkalosis.
The etiology is multifactorial:
- stimulation of distal tubule hydrogen ion secretion and
- hypokalemia-related acid-base effects,
- Contraction.
In addition to contraction alkalosis, such patients often have:
- renal bicarbonate generation due to elevated aldosterone levels,
- combined with generous distal tubule salt and water delivery.
- Hypokalemia also frequently contributes to accelerated renal bicarbonate generation and/or reduced renal bicarbonate excretory capacity.
- The GFR is usually reduced restricting the ability to excrete bicarbonate.
Emphysematous pyelonephritis: Rx
Antibiotics + percutaneous drainage
AKI: +anemia + hypercalcemia + diffuse bone pain
Meta: Multisystem DxProblem
Myeloma
HAGMA: Osmolal gap + AKI
Rx
Fomepizole + dialysis
Likely methanol or ethylene glycol poisoning
Comment: have not seen it
Goodpasture: Rx
Nephrotic syndrome: primary vs secondary: AetioClassification
- Primary:
- MCD
- FSGS
- MN
- Secondary:
- Diabetic
- Amyloidosis
- Lupus
Primary nephrotic syndromes include minimal change disease and focal segmental glomerulosclerosis (which primarily affect podocytes), as well as membranous nephropathy. Secondary nephrotic syndrome can occur as a result of systemic illnesses, including diabetes mellitus, amyloidosis, and lupus nephritis (class V membranous lupus nephritis or lupus nephritis with podocytopathy).
Nephrotic syndrome: features other than proteinuria
What other abnormalities often accompany the proteinuria, hypoalbuminemia, and peripheral edema that characterize the nephrotic syndrome?
- Hyperlipidemia
- Thrombophilia
The nephrotic syndrome affects both the biosynthesis and the clearance of lipoproteins and results in hyperlipidemia and alterations in the composition of lipoproteins; the severity of these effects is proportional to the degree of proteinuria. The nephrotic syndrome causes thrombophilia that results from an overall net increase in procoagulant factors due to a variety of different mechanisms.
FSGS: Collapsing variety
Q. What characterizes the collapsing variant of focal segmental glomerulosclerosis?
AKI + nephrotic syndrome presentation
Patients with the collapsing variant of focal segmental glomerulosclerosis often present with acute kidney injury in addition to the nephrotic syndrome. Collapsing focal segmental glomerulosclerosis is characterized by widespread podocyte injury with diffuse effacement of foot processes and severe proteinuria, as well as collapse and sclerosis of the entire glomerular capillary bed. This variant of focal segmental glomerulosclerosis contrasts with other variants, in which areas of mesangial collapse and sclerosis typically affect only a portion of the glomerular surface, sparing some glomeruli entirely and maintaining enough capillary surface area to preserve renal function during the early stages of this disease.
The causes of collapsing focal segmental glomerulosclerosis are varied. Several infections are associated with collapsing focal segmental glomerulosclerosis; human immunodeficiency virus (HIV)–associated nephropathy is a classic form of this condition.
It is thought that HIV directly infects podocytes, which leads to dedifferentiation, apoptosis, and widespread effacement of foot processes.
Nephropathy: HIV Nephropathy: Features
What are some of the features of human immunodeficiency virus (HIV)–associated nephropathy?
- Tubules: Microcystic dilatation
- Fill with proteinaceous material
- tubulointerstitial nephritis
- kidneys enlarged; echogenic USG
- 50%: progression to end-stage renal disease,
HIV-associated nephropathy classically occurs in patients with chronic, uncontrolled HIV infection and is associated with a CD4 cell count of less than 250 per cubic milliliter, but on rare occasions, it can also be seen as a manifestation of acute HIV infection.
HIV-associated nephropathy is also associated with characteristic histologic changes that affect each of the different renal compartments.
The tubules classically develop microcystic dilatation; they fill with proteinaceous material and undergo cast formation, and a lymphocytic infiltrate and tubulitis are commonly seen. Because of the tubulointerstitial nephritis and the proteinaceous, cast-filled microcysts, the kidneys become enlarged and appear echogenic on renal ultrasonography.
Approximately 50% of patients with HIV-associated nephropathy have progression to end-stage renal disease, and this highlights the need for a directed therapy for HIV-associated nephropathy that halts the progression of renal disease.
