Nephrology Flashcards
Isopropyl alcohol ingestion
Patients with isopropyl alcohol ingestion have altered mental status, elevated osmolar gap, normal anion gap, and ketonuria/ketonemia. Treatment is mainly supportive.
PTH dependant HyperCa
If urinary Ca >250mg / 24Hrs
⏩⏩ primary or tertiary hyperparathyroidism
If urinary Ca <100mg / 24Hrs
⏩⏩ Familial hypercalcemic hypocalciuria
Causes of hypercalcemia in patients with low PTH (independent)
Normal PTHrP, 25 & 1,25 Vit D
Hyperthyroidism
Multiple myeloma
Adrenal tumor
Acromegaly
Vitamin A toxicity
Immobilization
Milk-alkali syndrome
Acute interstitial nephritis
Causes
Medications (eg, antibiotics, NSAIDS, PPIs)*
Rheumatologic disease (eg, SLE, Sjögren syndrome,sarcoidosis)
Infections (eg, Legionella, tuberculosis, CMV)
Acute interstitial nephritis
Clincal presentation
New medication exposure, Acute kidney injury, Arthralgias, malaise
Classic triad of fever, skin rash & eosinophilia rarely
Urinalysis: WBCs & WBC casts + mild RBCs & proteinuria
Peripheral eosinophilia + urine eosinophils
Renal biopsy: tubulointerstitial inflammation & edema
Acute interstitial nephritis treatment
Offending medications should be discontinued immediately. Renal biopsy is diagnostic but is not required in patients whose renal function improves after medication withdrawal
Glucocorticoids are often used in patients who fail to improve after medication withdrawal, although the benefits remain unclear
Extrarenal complications of Adult polycystic kidney disease
• Intracranial aneurysms
• Hepatic and pancreatic cysts
• Cardiac valve disease and aortic root dilatation
• Diverticulosis
ADPKD, intracranial aneurysm screening
Guidelines recommend screening patients with previous aneurysm rupture, family history of intracerebral bleed or aneurysm, and high-risk occupations (eg, pilots).
screening is best performed with time-of-flight magnetic resonance angiography, which does not require gadolinium contrast and can be done at any glomerular filtration rate level.
Computed tomography angiography is an alternate screening method.
Causes of NAGMA
• Diarrhea
• Fistulae (eg, pancreatic, ileocutaneous, etc.)
• Carbonic anhydrase inhibitors
• Renal tubular acidosis
• Ureteral diversion (eg, ileal loop)
• Iatrogenic
Check Urine Anion gap
Positive ⏩ Renal cause
Negative ⏩ Gi cause
Toluene ingestion
Toluene is inhaled and then converted by the liver to hippuric acid, which can cause an elevated anion gap metabolic acidosis in the early stages.
However, hippuric acid is rapidly excreted by the kidneys along with sodium and potassium. There is also limited renal ammonium production and eventual distal RTA.
The resultant serum hypokalemia leads to diffuse weakness, low level of rhabdomyolysis, and hypophosphatemia. Treatment is largely supportive with fluid and electrolyte repletion
Salicylate toxicity
Presentation
encephalopathy
anion gap metabolic acidosis (AGMA) and an additional respiratory alkalosis.
auditory (eg, tinnitus with hearing loss), gastrointestinal (eg, gastritis, vomiting), and pulmonary (eg, noncardiogenic edema)
Salicylate toxicity
Management
1- involves serum and urinary alkalinization via intravenous bicarbonate administration even in the setting of alkalosis (as long as pH <7.60). Serum alkalinization promotes salicylate movement out of cells while urinary alkalinization increases the rate of renal excretion.
Acetazolamide should not be given; although it alkalinizes the urine, this occurs at the expense of serum acidification with a resultant salicylate movement into cells.
2-Hemodialysis should be considered in severe cases (eg, pulmonary or cerebral edema, renal failure).
Intubation should be avoided because adequate hyperventilation is difficult to maintain mechanically in these patients, and they are highly susceptible to worsening acidemia with a drop in minute ventilation
Creatinine and Bactrim
By decreasing creatinine secretion, both trimethoprim and cimetidine can result in an increased serum creatinine without decreasing the glomerular filtration rate.
Bk polyoma virus
Introduction
In renal transplant recipients, the BK form of polyoma virus produces tubulointerstitial nephritis and, less commonly, ureteric stenosis.
The mean time of onset of BK infection is 10-15 months after transplantation.
BK viral infection is most common in older men with type 2 diabetes mellitus and rejection episodes with significant immunosuppression.
There are no characteristic clinical manifestations other than loss of renal function.
Bk polyoma infection
Diagnosis and treatment
The presence of cells with a single large basophilic intranuclear inclusion found on urine cytology suggests but does not prove BK infection.
Serology is not as useful as many in the general population have antibodies against the virus.
Renal biopsy findings can be similar to those in other viral infections (eg, cytomegalovirus). As a result, diagnosis requires renal biopsy showing characteristic cytopathology plus positive antibodies directed specifically against BK on immunohistochemistry tests.
Biopsy sometimes misses the diagnosis, and at least 2 biopsy cores may be required in suspected patients.
The primary treatment is reduction of immunosuppression.
Calcineurin inhibitor nephrotoxicity
Patients can have declining glomerular filtration rates and a variety of metabolic abnormalities, including hyperkalemia, hyperuricemia, hypophosphatemia, hypomagnesemia, hypercalciuria, and possibly metabolic acidosis.
Significant hypertension may also be present. Toxicity is dose-dependent. Calcineurin inhibitors are metabolized by cytochrome P450 3A4; levels are increased by other drugs that are metabolized by this enzyme (eg, azole antifungals, macrolides, non-dihydropyridine calcium channel blockers).
Biopsy is often required to rule out acute rejection.
Acute calcineurin inhibitor toxicity is usually reversible with drug cessation, although some patients develop residual chronic renal dysfunction.
Nephrogenic DI
Lithium can be associated with nephrogenic DI in up to 20-40% of patients. Symptomatic patients should discontinue lithium. Patients who cannot stop lithium may be treated with salt restriction and a trial of diuretics (i.e., amiloride or thiazides) with careful monitoring of renal function and serum lithium levels.
CKD-MBD
Osteitis fibrosa cystica
Lab findings
• PTH >450 pg/mL
• High ALP
Treatment
Decrease PTH
• Dietary phosphate restriction, phosphate binders
• Vitamin D analogues
• Calcimimetics* i.e. cinacalcet in dialysis patients only
CKD-MBD
Adynamic bone disease
Lab findings
• PTH <100 pg/mL
• Low or normal ALP
Treatment
Increase PTH:
• Discontinue vitamin D analogues
• Switch to non-calcium- containing phosphate binders
• Use low-calcium dialysate in dialysis patients only
Contrast induced nephropathy prevention
Preventive measures include using the smallest possible volume of contrast media, holding nonsteroidal anti-inflammatory drugs, and optimizing volume status to maximize renal perfusion (ie, IV normal saline in most patients, diuretics if volume overload is present).
No role of holding ACE Is or ARBs prior contrast administration
Scleroderma renal crisis
Risk factors:
• Diffuse, aggressive skin involvement, tendon friction rubs
• High-dose glucocorticoid therapy
• Anti-RNA polymerase III antibodies (lower risk with anticentromere antibodies)
Presentation:
• Acute kidney injury
• Moderate or severe hypertension/malignant hypertension
• Proteinuria, normal urine sediment
• Microangiopathic hemolytic anemia
Treatment:
Oral ACE Inhibitors captopril, back to baseline within 72Hrs
Post obstruction diuresis
Chronic partial bilateral urinary obstruction can result in normal or slightly increased urine volume, while complete bilateral obstruction causes anuria. Relief of the obstruction leads to post-obstructive diuresis (500-1000 cc/hr) that can be worsened by trying to match volume repletion with urine output.
There are no controlled studies to guide management; however, most experienced clinicians replace the patient’s body volume with either isotonic or half normal saline at a rate <50% of urine volume (eg, ~200 cc/hr in this patient with urine output ~600 cc/hr) and adjust the rate based on the patient’s response and subsequent volume status
Hyperphosphatemia &FGF 23
FGF-23, the major phosphaturic hormone. FGF-23 decreases the expression of the sodium phosphorous cotransporter in the proximal tubule. In tumoral calcinosis, FGF-23 activity is decreased; therefore, there is increased phosphorous absorption in the proximal tubule resulting in hyperphosphatemia and metastatic calcifications
Mild microscopic hematuria
The presence of isolated dysmorphic hematuria in a young patient typically indicates very mild glomerular disease (most often IgA nephropathy) or thin glomerular basement membrane disease related to a type IV collagen defect. Thin glomerular basement membrane disease is more likely if there is a strong family history of hematuria, which is found in 30% to 50% of cases, and no family history of chronic kidney disease.
