RENAL Flashcards
_% of our lean body mass is made up of our TBW
65% of lean body mass is made up of TBW
ECF: 20-25% of TBW
> Interstitial fluid: 15%
> Plasma: 5%
ICF: 30-40% of TBW
ECF: _% of TBW
ICF: _% of TBW
65% of lean body mass is made up of TBW
ECF: 20-25% of TBW
> Interstitial fluid: 15%
> Plasma: 5%
ICF: 30-40% of TBW
Consequence of hyponatremia
Brain swelling
Brain cell swelling is responsible for most of the symptoms of hyponatremia. Neurologic symptoms of hyponatremia include anorexia, nausea, emesis, malaise, lethargy, confusion, agitation, headache, seizures, coma, and decreased reflexes. Patients may have hypothermia and Cheyne-Stokes respirations. Hyponatremia can cause muscle cramps and weakness; rhabdomyolysis can occur with water intoxication.
Consequence of hypernatremia
Brain hemorrhage
Consequence of rapid correction of hyponatremia
Central pontine myelinosis (CPM)
Osmotic demyelinating syndrome
CPM is more common in patients who are treated for CHRONIC hyponatremia than in those treated for acute hyponatremia. Presumably, this difference is based on the adaptation of brain cells to the hyponatremia. The reduced intracellular osmolality that is an adaptive mechanism for chronic hyponatremia makes brain cells susceptible to dehydration during rapid correction of the hyponatremia, and this may be the mechanism of CPM. Even though CPM is rare in pediatric patients, it is advisable to avoid correcting the serum sodium concentration by >12 mEq/L/24 hr or >18 mEq/L/48 hr.
Correction of hyponatremia must not exceed _
10meqs/L/24hrs OR not more than 18meqs/L/48hrs (Nelson)
Correction of hypernatremia _
by <10meqs/L/24hrs (Nelson)
<12meqs/L/24hrs
Hyperkalemia correction
GICKS-L
- Glucose
- Insulin
- Calcium gluconate - WILL NOT DEC POTASSIUM BUT WILL STABILIZE THE HEART
- Kayexelate
- Salbutamol / Steroids
- Lidocaine / Loop diuretics
Frequent etiology of acute hemorrhagic cystitis
> Frequently caused by E. coli
RARE in children
Pyelonephritis characterized by giant cells and histiocytes
A. Acute hemorrhagic cystitis
B. Eosinophilic cystitis
C. Xanthogranulomatous pyelonephritis
D. Interstitial cystitis
C. Xanthogranulomatous pyelonephritis
Causes of FALSE NEGATIVE hematuria on dipstick
Presence of formalin and high urinary concentration of Vitamin C
Causes of FALSE POSITIVE hematuria on dipstick
Alkaline urine (pH >8)
(same for proteinuria)
Most common chronic glomerular disease in children
IgA Nephropathy
> predominance of IgA within mesangial glomerular deposits in the absence of a systemic disease
Primary treatment of IgA nephropathy (2)
- Control BP
- Proteinuria management
BP medications for IgA Nephropathy
ACEi and ARBs
> effective in reducing proteinuria and retarding the rate of disease progression when used individually or in combination
If ACEi and ARBs fail- add corticosteroids
> reduce proteinuria and improve renal
function in those patients with a glomerular filtration rate >60 mL/min/m2.
Acute post-strep GN:
1. Hypertension resolves _ wks after infection
2. Proteinuria resolves _
3. Hematuria is persistent _
4. Serum C3 resolves after _
> Urinary protein excretion and hypertension usually normalize by 4-6 wk after
persistent microscopic hematuria can persist for 1-2yr after the initial presentation.
Serum C3 normalizes after 6-8wks
Classic histopathologic finding in HIV-associated nephropathy
Focal segmental glomerulosclerosis
FALSE NEGATIVE RESULTS FOR PROTEINURIA (3)
- Low pH (<4.5)
- Diluted urine (sp <1.005) or large volume of UO
- Disease states in which predominant protein is NOT albumin
FALSE POSITIVE RESULTS FOR PROTEINURIA (5)
- High pH >7.0
- Highly concentrated urine
- Contamination w blood
- Presence of pyuria
- Prolonged dipstick immersion
Features of NEPHROTIC syndrome (4)
EPAL
1. Edema (most common presenting symptom)
2. Proteinuria (>40mg/m2/hr or >3.5g/24hr or UPCR >2-3)
3. Albuminemia (hypo, <2.5g/dl)
4. Lipidemia (hyper, cholesterol >200mg/dL)
Most common cause of nephrotic syndrome in children
Minimal Change Disease
> most are steroid-sensitive
Mainstay treatment of Minimal Change Disease.
Alternative treatment? (6)
Prednisone: 2mkday or 60mg/m2/day single daily dose for 4-6 weeks.
Taper to 15mkday or 40mg/m2/day alternate every other day.
> 80-90% respond in 3 weeks
> Majority will respond after 5 weeks
Alternative Treatment:
1. Cyclophosphamide
s/e: Neutropenia
2. Calcineurin inhibitors (Tacrolimus, Cyclosporine)
3. Mycophenolate mofetil
4. Levasimole
5. Rituximab
6. AEi ARBs
Calcineurin & MMF- once discontinued, can cause proteinuria
If failure to treat Minimal Change Disease w steroids, most likely cause of nephrotic syndrome is now _.
Focal Segmental Glomerulosclerosis (80%)
> 50% risk for ESRD
When can you give live vaccines to children w Nephrotic Syndrome?
When Prednisone dose is <1mkday or 2mg/kg alternate day
Contraindicated if children is on Cylosporine or cyclophosphamide.
Household contacts highly recommended to get live vaccines - but avoid immunocompromised patients for 3-6weeks.
Children with nephrotic syndrome should receive the 23-serotype pneumococcal vaccine (in addition to the 7-valent conjugate pneumococcal vaccine), given according to the routine childhood immunization schedule, ideally administered when the child is in remission and off daily prednisone therapy.
Live virus vaccines should NOT be administered to children who are receiving daily or alternate-day high-dose steroids (≥2 mg/kg/day of prednisone or its equivalent, or ≥ 20 mg/day if the child weighs > 10 kg). Vaccines can be administered after corticosteroid therapy has been discontinued for at least 1 mo. Nonimmune nephrotic children in relapse, if exposed to varicella, should receive varicella-zoster immunoglobulin (1 dose ≤ 96 hr after significant exposure). Influenza vaccine should be given on a yearly basis.
Definitive treatment for Congenital Nephrotic Syndrome
Kidney transplant
Most common manifestation in target-organ damage in childhood hypertension
Left ventricular hypertrophy
_ account for 90% of children with secondary hypertension.
Renal disease and renovascular hypertension
Goal BP in hypertensive crisis
BP reduction NOT MORE THAN 25% in the first 8hrs
> Short-term goal is bP around 95th percentile
Goal BP in childhood hypertension (2)
- Achieve BP <90th percentile for age, or <130/80; whichever is lower
- For children w CKD, MAP of <50th percentile
Metabolic Acidosis
Normal AG:
High AG:
Normal AG: HARDUP
> Hyperalimentation
> Acetazolamide, adrenal insufficiency
> RTA, Renal insufficiency
> Diarrhea/diuretics
> Uteroenterostomy
> Pancreatic fistula
High AG: MUDPILES
> Methanol
> Uremia
> DKA
> Paraldehyde
> INH, iron, inhalants
> Lactic acid
> Ethanol/ethylene glycol
> Salicyclates, starvation, solvents (toluene)
Indomethacin is used in _ (3)
- Congenital nephrotic syndrome - decrease proteinuria
- Bartter syndrome (Type 2 is sensitive to indomethacin)
- Nephrogenic Diabetes Insipidus - increase water reabsorption in terminal segments
HUS triad
RMT
1. Renal failure
2. Microangiopathic hemolytic anemia
3. Thrombocytopenia
Most common type of Lupus Nephritis
Type IV - diffuse proliferative glomerulonephritis
> Poorer prognosis
Most common cause of AKI in children
Hemolytic Uremic Syndrome
> caused by Shiga Toxin producing E. coli (O157:H7) - STEC HUS
> Non STEC: Shigella dysenteriae Type 1
Most common benign solid tumor of the kidney
Angiomyolipoma
A 14yo female presents with urgency associated with bladder and pelvic pain relieved by voiding. Urine culture is negative. Primary consideration is:
A. Acute hemorrhagic cystitis
B. Eosinophilic cystitis
C. Interstitial cystitis
D. Xanthogranulomatous nephritis
C. Interstitial cystitis
KEYWORDS:
> Relieved by voiding
> Urine culture negative; idiopathic
A 4mos old male w high grade fever asstd w vomiting. On PE, irritable, febrile, with SS of DHN.
UA reveals pyuria. Pending Urine CS, the most appropriate antibiotic to give is:
A. Amoxicillin
B. Ceftriaxone
C. Nitrofurantoin
D. Ofloxacin
B. Ceftriaxone - 3rd gen Cephalosporins
A. Amoxicillin - high resistance
C. Nitrofurantoin - no significant tissue levels
D. Ofloxacin - reserve for Pseudomonas infx
A 2yo female comes in w CC of foul-smelling urine. She would strain on urination. No fever or vomiting. Urinalysis reveals pyuria. What is the most appropriate to give while pending urine CS results?
A. Ampicillin
B. Ceftriaxone
C. CoAmoxiclav
D. Ofloxacin
C. CoAmoxiclav
KEYWORDS:
> Lower UT symptoms: Strain
> Pyuria on UA
> NO fever or vomiting
CYSTITIS- oral antibiotics will suffice
> No renal injury
Indications for chemoprophylaxis for UTI (4)
VNSC
1. Severe VUR
2. Neuropathic bladder
3. urinary Stasis and obstruction
4. urinary Calculi
> TMP-SMX, NFT, Nalidixic acid
PPS Statement on factors that can reduce UTI (2)
- Breastfeeding
- Circumcision
Potential causes of hyperkalemia include all of the following EXCEPT:
A. Succinylcholine administration
B. Digitalis toxicity
C. Spironolactone use
D. Albuterol overdose
E. Yasmin use
D. Albuterol overdose
Normal doses of succinylcholine or digitalis intoxication all cause a shift of potassium out of the intracellular compartment. Succinylcholine should not be used during anesthesia in patients at risk for hyperkalemia. Potassium-sparing diuretics may easily cause hyperkalemia, especially because they are often used in patients who are receiving oral potassium supplements. The oral contraceptive Yasmin-28 contains drospirenone, which blocks the action of aldosterone.
Manifestations of hyperkalemia include all of the following EXCEPT:
A. Paresthesias
B. Weakness
C. Paralysis
D. Wide QRS complex
E. Tetany
E. Tetany
The most important effects of hyperkalemia are due to the role of potassium in membrane polarization. The cardiac conduction system is usually the dominant concern. Changes in the electrocardiogram (ECG) begin with peaking of the T waves. This is followed, as the potassium level increases, by ST segment depression, an increased PR interval, flattening of the P wave, and widening of the QRS complex. This process can eventually progress to ventricular fibrillation. Asystole may also occur. Some patients have paresthesias, fasciculations, weakness, and even an ascending paralysis, but cardiac toxicity usually precedes these clinical symptoms, emphasizing the danger of assuming that an absence of symptoms implies an absence of danger.
Hyperkalemia may be associated with all of the following EXCEPT:
A. Succinylcholine use
B. Burns
C. Trauma
D. Chemotherapy
E. Metabolic alkalosis
F. Digitalis toxicity
G. Uremia
E. Metabolic alkalosis
Many causes of hyperkalemia result in metabolic acidosis; a metabolic acidosis worsens hyperkalemia through the transcellular shift of potassium out of cells. Renal insufficiency is a common cause of the combination of metabolic acidosis and hyperkalemia. This association is also seen in diseases associated with aldosterone insufficiency or aldosterone resistance.
Which statement regarding hypermagnesemia is NOT true?
A. Hypermagnesemia may cause hypertension and hyporeflexia
B. Pediatric hypermagnesemia most commonly occurs in neonates born to mothers with preeclampsia or eclampsia requiring treatment with IV magnesium
C. Excessive laxative use may cause hypermagnesemia
D. Hypermagnesemia may be treated with IV fluids and loop diuretics
E. Infants with hypermagnesemia have a poor suck
A. Hypermagnesemia may cause hypertension and hyporeflexia
Hypermagnesemia inhibits acetylcholine release at the neuromuscular junction, producing hypotonia, hyporeflexia, and weakness; paralysis occurs at high concentrations. The neuromuscular effects may be exacerbated by aminoglycoside antibiotics. Direct CNS depression causes lethargy and sleepiness; infants have a poor suck. Elevated magnesium values are associated with hypotension because of vascular dilation, which also causes flushing. Hypotension can be profound at higher concentrations from a direct effect on cardiac function. Most patients with normal renal function rapidly clear excess magnesium. Intravenous hydration and loop diuretics can accelerate this process. In severe cases, especially in patients with underlying renal insufficiency, dialysis may be necessary.
Possible consequences of hypophosphatemia include all of the following EXCEPT:
A. Hypocalcemia
B. Hemolysis
C. Rhabdomyolysis
D. Paresthesias
E. Seizures
A. Hypocalcemia
Severe hypophosphatemia, typically at levels <1-1.5 mg/dL, may affect every organ in the body because phosphorus has a critical role in maintaining adequate cellular energy. Severe hypophosphatemia can cause hemolysis and dysfunction of white blood cells. Chronic hypophosphatemia causes proximal muscle weakness and atrophy. In the intensive care unit, phosphorus deficiency may slow weaning from mechanical ventilation or cause acute respiratory failure. Rhabdomyolysis is the most common complication of acute hypophosphatemia, usually in the setting of an acute transcellular shift of phosphorus into cells in a child with chronic phosphorus depletion (anorexia nervosa). The rhabdomyolysis is actually somewhat protective, in that there is cellular release of phosphorus. Other manifestations of severe hypophosphatemia include cardiac dysfunction and neurologic symptoms, such as tremor, paresthesia, ataxia, seizures, delirium, and coma. Hyperphosphatemia causes hypocalcemia and systemic calcification.
From the following list, choose the route(s) by which insensible water loss may occur: 1. Sweat, 2. Fecal loss, 3. Evaporative loss from skin, 4. Respiratory water loss, 5. Obligate water for urinary solute excretion
- Evaporative loss from skin AND 4. Respiratory water loss
Water is a crucial component of maintenance fluid therapy because of the obligatory daily water losses. These losses are both measurable (urine, stool) and not measurable (insensible losses from the skin and lungs). Failure to replace these losses leads to a child who is thirsty, uncomfortable, and, ultimately, dehydrated.
Serious complications hypernatremic dehydration, including its treatment, include:
A. Cerebral thrombosis
B. Cerebral edema
C. Cerebral hemorrhage
D. A and B
E. All of the above
E. All of the above
Hypernatremic dehydration is the most dangerous form of dehydration due to complications of hypernatremia and of therapy. Hypernatremia can cause serious neurologic damage, including central nervous system hemorrhages and thrombosis. This damage appears to be secondary to the movement of water from the brain cells into the hypertonic extracellular fluid, causing brain cell shrinkage and tearing blood vessels within the brain. Hypernatremia may cause fever, hypertonicity, and hyperreflexia. More severe neurologic symptoms may develop if cerebral bleeding or thrombosis occurs. With overly rapid lowering of the extracellular osmolality during the correction of hypernatremia, an osmotic gradient may be created that causes water movement from the extracellular space into the cells of the brain, producing cerebral edema. Symptoms of the resultant cerebral edema can range from seizures to brain herniation and death.
A 2 yr old girl has an acute afebrile diarrheal syndrome characterized by abdominal pain, vomiting, and grossly bloody stools. A stool culture on MacConkey sorbitol media suggests E. coli O157:H7; a fecal toxin electroimmunoassay suggests that a Shiga toxin is present. Appropriate care includes:
A. Loperamide
B. An oral antibiotic (choice based on susceptibility of the Shiga toxin-producing E. coli)
C. A parenteral antibiotic (choice based on susceptibility of the Shiga toxin-producing E. coli)
D. Careful follow-up evaluation for development of thrombocytopenia, anemia, and/or renal failure
D. Careful follow-up evaluation for development of thrombocytopenia, anemia, and/or renal failure
There is no evidence that any therapy directed at arresting the disease process of the most common, diarrhea-associated form of HUS provides benefit, and some can cause harm. Attempts have been made using anticoagulants, antiplatelets agents, fibrinolytic therapy, plasma therapy, immune globulin, and antibiotics. Anticoagulation, antiplatelet, and fibrinolytic therapy is specifically contraindicated because it increases the risk of serious hemorrhage. Antibiotic therapy to clear the toxigenic organisms can result in increased toxin release, potentially exacerbating the disease, and therefore is not recommended. Prompt treatment of any underlying pneumococcal infection is important. Attempts to bind verotoxin or Shiga toxin in the gut to prevent systemic absorption, and thereby prevent or ameliorate the course of HUS, have been unsuccessful in extensive controlled clinical trials.
Immunofluorescent histologic finding that is diagnostic of Lupus nephritis
Granular deposition of ALL IG isotypes (IgG M A) and complements (C3 4 and C1q) in the glomerular mesangium.
> full-house immune staining
IgA Nephropathy vs Henoch Schonlein Purpura nephritis
IgA vs PSGN
IgA: URTI together with hematuria (within 1-2 days of URTI). Normal complement levels
HSP: Purpuricrash, arthralgia/arthritis, abdominal pain, nephritis AFTER URTI.
PSGN: 3-6wks post-infection. Decreased C3 levels
Classic tetrad of HSP nephritis.
- Palpable rash
- Abdominal pain
- evidence for renal disease
- Arthritis or arthralgia
Not all tetrad are present in all patients
Classic presentation of acute tubulointerstitial nephritis (3)
- Fever
- Rash
- Arthralgia
WITH INCREASING SERUM CREATININE.
> Most commonly caused by use of NSAIDs in children, w dehydration
Indications for dialysis in AKI (7)
AEIOU
(Acidosis, anuria, electrolyte, intoxication, fluid overload, uremia)
- Anuria/oliguria
- Volume overload w evidence of HTN and/or pulmonary edema refractory to diuretic therapy
- Persistent hyperkalemia
- Severe metabolic acidosis, unresponsive to medical management
- Uremia - enceph, pericarditis, neuroptahy
- Calcium:phosphorous imbalance, with hypocalcemic tetany that cannot be controlled by other measures
- Inability to provide adequate nutritional intake
Principal hormone regulating potassium secretion __
Aldosterone
