1.

RENAL
Monday, 31 January 2022 10:36 PM

Mnemotechnics.

• Clearance
○ C=UV/P. (Urinary concentration, Urinary volume and P is plasma concentration of
substance)
○ FF=GFR/RPF
§ RPF is measured with PAH

• PSGN contain IC visible on IF microscopy as granular deposits of IgG, IgM and C3. Because the
particular IC tend to activate complement via the alternate pathway, the deposits rarely conta
C1q or C4 (classic complement pathway complements).
○ PSG is caused by an streptococcal infection (eg impetigo, cellulitis, pharyngitis)

Uworld

• Membranoproliferative glomerulonephritis is typically caused by immune complex deposition

within the glomerular capillary walls and mesangium and can be associated with chronic infect
(eg, hepatitis B). It is characterized by large, hypercellular glomeruli with thickened capillary
walls. Immunofluorescence typically shows a granular pattern of IgG and C3. Electron microsc
shows subendothelial and mesangial deposits.
• Renal tubular acidosis : Kindeys do not remove acid from blood
○ Distal (RTA I) -> inhablity of alfa intercaleted cells to secrete H. Caused by amotericin B,
analgesic neephropathy, SLE. Increased risk of kidney stones
○ Proximal (RTA II): Casued by fanconi syndrome, multiple myeloma, carbonic anhydrase
inhibitors. Increased risk for hypophosphatemic rickets.
○ Hyperkalemic tubular (RTA IV) -> hypoaldosteronsim or aldosterone resistance.

• Normal temperature anywhere from 97F to 99F (36.1-37.2C)

• Heroin and opioids cause pinpoint pupils

○ Remember opioid cause respiratory depression (respiratory acidosis)
Heroin is associated with FSGS
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• Apuntes
 • Normal temperature anywhere from 97F to 99F (36.1-37.2C)

• Heroin and opioids cause pinpoint pupils

○ Remember opioid cause respiratory depression (respiratory acidosis)
○ Heroin is associated with FSGS
• Cocaine cause dilated pupils

Embryology Anatomy Histology

• Kidney development:
○ Nephrogenic cord forms pronephros, mesonephros and metanephros
○ Metanephric blastema: Glomeruli yo DCT
○ Metanephric diverticulum (ureteric bud): collecting tubules to ureters
• Straw collored discharge from umbilicus --> urachus (remanent of allantois), bladder
• Sequence: causa-and-effect- relationship (e.g. Potter syndrome)
• In AIN edema, significant hematuria and proteinuria are uncommon, usually it stops when dru
discontinued
• Urinary incontinence:
○ Stress 'pee when moving"
○ Urge " strong sense of urge". Stroke, parkinson, spinal cord injury, multiple sclerosis
○ Overflow "full and it's spilling over". Diabetic neuropathy, multiple sclerosis, spinal cord
injury
• Pupils constricted but reactive to light (nausea, diaphoresis, flushing, decreased HR) -> choline
agonist (mimic Ach), used to treat atonic bladder.
• Kegel exercise (pelvic floor) --> to strengthen levator ani muscle complex (iliococcygeus,
pubococcygeus, puborectalis)
• Ureter cross posterior to gonadal vessels, over iliac vessels and under uterine artery, vas
deferens.
• Anti-GMB disease (linear deposits IF)--> Goodpasture (collagen IV) --> RPGN (Type I)
• Horseshoe kidney is a congenital anomaly in which fusion of the metanephros (specifically,
metanephric blastema)

Physiology, pathophysiology

• Multiple myeloma (MM) is a plasma cell malignancy that generates monoclonal

immunoglobulin. It is classically characterized by anemia (normocytic), bone pain/radiolucent
lesions, and hypercalcemia due to tumor infiltration of the bone marrow. Suspect MM in
elderlies with these findings, renal failure can also be.
• Hyperphosphatemia causes hypocalcemia (sush in CKD).
• Celiac disease -> Malabsorption DEKA -> Vita D deficiency (rickets in children and osteomalaci
adults) -> PTH elevation -> Increase Ca+, decrease serum PO3-.
Vit D increase intestinal absorption of Ca and PO3-, also inhibits PTH release.
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 lesions, and hypercalcemia due to tumor infiltration of the bone marrow. Suspect MM in
elderlies with these findings, renal failure can also be.
• Hyperphosphatemia causes hypocalcemia (sush in CKD).
• Celiac disease -> Malabsorption DEKA -> Vita D deficiency (rickets in children and osteomalaci
adults) -> PTH elevation -> Increase Ca+, decrease serum PO3-.
○ Vit D increase intestinal absorption of Ca and PO3-, also inhibits PTH release.
○ PTH releases Ca and PO3- from bones
○ However VitD deficiency has low serum CA and PO3- and elevated PTH because PTH
stimulates PO3- renal excretion and initially PTH will maintain normal serum calcium
levels by reducing urinary calcium excretion but hypocalcemia may eventually develop
bone stores are depleted in later or more severe cases.

• PHPT besides kidney stones, classic manifestiations include bone pain, GI disturbances (peptic
ulcer disease) and psychiatric symptoms.
• Clacium and phosphate are regulated by PTH and VitD:
○ PTH increases ostoclastic bone resoprtion, increases renal calcium reabsoption, decrease
phosphate reabosorption and increases formation of 1,25 dihydroxyvitD.
§ PCT -> Decreased reabsorption of PO4 (most important)
§ DCT -> Increased reabsorption of Ca
○ Vit D: Increases Ca+ and PO4- absorption in GI (major mechanis of clinical effects) and
increases bone Ca+ and PO4 resorption
○ FGF23 is secreted by osteocytes in response to hyperphosphatemia (marker of
hyperphosphatemia) leading to reduce levels of 1,25hydroxyVitD (decrease intestinal
phosphate absorption and decrease renal phosphate reabsorption). Inititally in CKD it
maintains phosphate levels.
• Hypophosphatemia induces hypocalcemia (1 phosphate binds free calcium and precipitates in
soft tissues --> vascular aclcification and 2increased phophate triggers release of FGF-23 which
reduces production of 1,25hdroxyVitD in kidney)
○ Hypoparathyroidism is usually due to autoimmune disease or iatrogenic injury. It's not a
common finding in CKD.
• Hyperphosphatemia --> vascular calcifications
• Mild hypercalcemia is usually due to benign cause (primary hyperPTHA), but >13mg/dl sugges
underlying malignancy (Humoral hypercalcemia of malignancy -> PTH -related protein). Unlike
PTH, PTHrP does not significantly increase 1,25hidroxyVityD production.
• Diabetes with decreased aldosterone effect --> impaired renin secretion (juxtaglomerular
apparatus destruction) --> K+ excretion decreased but sodium Na normal due to ADH adjustme
• Endothelin 1 is a potent vasoconstrictor
• Diabetes: one of the earliest derangements that contributes to the pathogenesis of diabetic
neuropathy is an increase in the filtered glucose load (increased GFR).
• Cystine, ornithine , lysine and arginine (cola) share a common transporter in the intestine and
kidneys. In patients with cystinuria this transporter is defective --> cannot reabsorbe cysteine
kidney stones
• Certain tumors (small cell lung carcinoma, head and neck cancer) produces ADH--> SIADH
○ SIADH-> Serum sodium, serum osmolality, urine osmolality, and urine sodium are low.
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 neuropathy is an increase in the filtered glucose load (increased GFR).
• Cystine, ornithine , lysine and arginine (cola) share a common transporter in the intestine and
kidneys. In patients with cystinuria this transporter is defective --> cannot reabsorbe cysteine
kidney stones
• Certain tumors (small cell lung carcinoma, head and neck cancer) produces ADH--> SIADH
○ SIADH-> Serum sodium, serum osmolality, urine osmolality, and urine sodium are low.
• B adrenergic hyperactivity (cocaine) can cause acute hypokalemia because there is potassium
shift intracellularly
• Peritubular interstitial cells produce erythropoietin.
• When potassium increases the pH decreases.
• Reabsorption of Na+ stimulates K excretion (for example azetazolamide stimulates distal
reabsorption of Na+)
• AINES decrease GFR.
• Loss of epithelial cell polarity occurs early in ATN
• Creatinine clearence overstimates the GFR by approximately 10-20%

• Incontinence:
○ In multiple sclerosis you may have urge incontinence due to uninhibited bladder
contraction.
• In patients with primary polydipsia, excessive water intake often leads to
mild hyponatremia. In contrast, primary ADH deficiency in DI leads to free water loss
often with ensuing hypernatremia. In certain patients, water deprivation testing may b
helpful for differentiating PP from DI.
• Primary polydipsia --> polyuria with low urine osmolality (leads to mild hyponatremia).
○ After 8 hours of fluid rstriction urine should be concentrated (if dilute --> ineffective/abs
ADH).
• Diabetes insipidus:
○ Central diabetes insipidus --> ADH deficiency
○ Nephrogenic DI --> unresponsiviness of kidneys to ADH.
§ In adults usually due to lithium, in children mutations in V2.
§ Tto: thiazides (paradoxically it appear to reduce renal water loss in NDI inducing m
volume depletion that increases Na and H2O resorption in PCT).
○ Production of dilute urine. Deprivation test with desmopress indifferentiate central and
nephrogenic.
○ In DI, the highest osmolarity is achieved in the junction between the ascending and
descending limbs of the loop of Henle.

• Secondary hyperaldosteronism (renin tumor, renal artery stenosis, diuretic use, etc) --> elevat
renin and aldosterone
• Primary hyperaldosteronism --> high aldosterone but negative renin feedback (low renin)

• Altered consciousness, pinpoint pupils, decreased breath sounds and history of IV drug use sug
acute opioid overdose.
• Thick and thing ascendign limbs of Henle's loop and early DCT are impermeable to water.
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• Primary hyperaldosteronism --> high aldosterone but negative renin feedback (low renin)

• Altered consciousness, pinpoint pupils, decreased breath sounds and history of IV drug use sug
acute opioid overdose.
• Thick and thing ascendign limbs of Henle's loop and early DCT are impermeable to water.

• Infusion of excess saline infusion (even isotonic) --> non anion gap metabolic acidosis

The rest of the subjects except pharmacology

• Elevated creatine kinase -> rhabdomyolysis, it causes ATN (granular, myddy brown) due to tub
injury due to increased myoglobulin. Urine dipstick reagent detects hemoglobin, leading to fals
positive result of blood in urine.
○ Asociate rhabdomyoltsis with prolongued muscle activity (seizure, marathon, exercise)

• Renal amoniagenesis is a process by which renal epithelial cells metabolize glutamine generat
ammonium and bicarbonate.
• Wilson disease is treated with penicillamine which can cause membranous nephropathy.
• Altered mental status+acute renal failure+ oxalate crystals -> ethylene glycol poisoning -> ATN
• Vomiting -> hypokalemic, hypochloremic metabolic alkalosis.
• Hypertensive nephrosclerosis is a common compilation of chronic hypertension.
• ATN cased by a drug usually occurs after a prolonged course (days), it's highly unlinkely that a
single dose would cause ATN.
• GN is a commmonly manifestation of small vessel vasculitis SVV, which usually has associated
systemic symptoms (eg, fever, fatigue).
• Ischemic ATN primarily affects the corticomedullary junction and the outer medulla
• Back pain, fatigue, normocytic anemia, renal failure, and gamma gap (serum total protein minu
serum albimin >4g/dl) likley has multiple myeloma).
• Henoch-Schönlein purpura is an IgA-mediated, leukocyotoclastic vasculitis that presents with
palpable purpura, arthralgia/arthritis, abdominal pain and or hematuria. Renal involvement is
to mesangial deposition of IgA IC with subsecuent mesangial cell proliferation, neutrophilic
infiltration and glomerular damage.
○ Henoch-Schonlein Purpura (IgA vasculitis): Skin (palpable purpura on the buttocks and
lower extremities), GI ( colicky abdominal pain, bowel wall edema and hemorrage can a
lead to GI bleeding), Kidneys ( microscopic hematuria), Joints (transient or migratory
arthralgia or arthritis).

• 85% of renal cell carcionma is clear cell carcinoma CCC, it originates form the epithelium of PC

• Hereditary vitamin D resistant rickets (HDVRR): Ca low , Phosphurus low, 25 HydroxyVitD low a
1,25 HydroxyvitD high (because lack of Vit D-> hypocalcemia -> high PTH -> alpha 1 hydroxylas
activity increased).
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• 85% of renal cell carcionma is clear cell carcinoma CCC, it originates form the epithelium of PC

• Hereditary vitamin D resistant rickets (HDVRR): Ca low , Phosphurus low, 25 HydroxyVitD low a
1,25 HydroxyvitD high (because lack of Vit D-> hypocalcemia -> high PTH -> alpha 1 hydroxylas
activity increased).

• Enlarged nontender prostate raises strong suspicious BPH. Microscopic or gross hematuria can
sometimes arise in patients with BPH due to the formation of new, friable blood vessels in the
area of the prostatic hyperplasia. You can have increased detrusor wall trabeculations due to
detrusor muscle hypertrophy. In BHP kidneys can develop hydronephrosis and renal parenchy
atrophy.
• NSAIDS (ibuprofen) can cause renal failure (analgesic nephropathy), prolonged use results in
chronic interstitial nephritis visualized as patchy interstitial inflammation with subsequent tub
atrophy and fibrosis, papillary necrosis and scarring pathologic findinds typically include papilla
necrosisis and tubulointerstitial nephritis).
• Analgesic nephropathy include chronic intersitial nephritis and papillary necrosis.
• Adult onset is poor prognosis for PSGN.
• AA amyloidisis results from excessiv serum amiloid A produced in rhematoid arthritis and oth
chronic inflmmatory conditions. After biopsy the serum protein electrophoresis test would be
helpful diagnostic test.
• IVC obstruction -> bilateral lower extremity pitting edema and tortous abdominal veins.
• Membranous nephropathy -> SLE. diffuse thickening of GBM that resemble spikes and omes
when stained with a silver stain
• TTP -> pentad of fever, nerologico symptoms, renal failure, anemia, thrombocytopenia
• SLE -> Glomerulonephritis (HTA, renal failure, proteinuria, RBC casts) + transitient arthralgias,
uclers and cytopenia
• BPH with acute urinary retention is associated with UTI
• Most important prognosis in urothelial carcinoma is based on the depth of invasion.
• Diarrhea (often bloody), hemolytic anemia with schistocyes, thrombocytopenia, acute kiney
injury -> HUS.
• Livdeo reticularis, a blue toe and acute kidney injury following coronary angiography is a
presentation concernign for atheroembolic disease.
• Gross hematuria and sickle cell disease --> renal papillary necrosis.
○ Gross hematuria --> papillary necrosis
• Scleroderma renal crisis ( complicetion of systemic scelrosis) cases immune-mediated injury to
small renal vessels that typically spares the glomerular capillaries.
• Fibrosis and strictures are late effects of radiation therapy. Radiotherapy for prostate cancer m
lead to urethral fibrosis and result in obstructive uropathy.
• Citrate for preventing calcium stones (oxalate, phosphate).
• Transient arthralgias, oral ulcers and cytopenia suggest SLE complicated by lupus nephritis (IC
containing DNA and anti DNA) <8deopsition fo IC containing DNA and anti-DNA). You cn also h
elevated HTA and creatinine, proteinuria and RBC casts.
• Renal infarction -> flank pain, low grade fever and hematuria (watch out patients with
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 • Citrate for preventing calcium stones (oxalate, phosphate).
• Transient arthralgias, oral ulcers and cytopenia suggest SLE complicated by lupus nephritis (IC
containing DNA and anti DNA) <8deopsition fo IC containing DNA and anti-DNA). You cn also h
elevated HTA and creatinine, proteinuria and RBC casts.
• Renal infarction -> flank pain, low grade fever and hematuria (watch out patients with
cardioembolic disease like atrial fibrillation). Hypertension can occure due to renin release form
hypoxic tissue.
• Alfa-2 macroglobulin levels increased when serum albumin levels are low (nephrotic syndrom
• Painless gross hematuria in an older patients raises suspicions of urothelial (transitional) blad
cancer.(usually prostate cancer is typically asymptomatic or discovered on evlauation of luwe
urinary trat symptoms). Major risk factors include cigarette smoking and occupational exposur
rubber, plastics.
• Aminoglycosides (gentamicin) related with acute tubular necrosis (granular casts) more than
with acute interstitial nephritis. The clinical course of ATN may be divided into the initiation
(24-36h), maintenance (oliguric, 1-2 weeks) and recovery phases (re-epithelization of tubules).
○ In ATN GFR often improves before renal tubular resorption function is restored, so patie
can develop transient polyuria with significant electrolyte wasting, during this time patie
are at high risk for developing hypokalemia.
• Acute interstitial nephritis has pyuria (classically eosinophils) and is associated with fever, rash
hematuria, costovertebral angle tenderness but can be asymptomatic.
• Fibromuscular dysplasia -> abnormal tissue growth within arterial walls, resulting in stenotic a
tortuous arteries that can cause ischemia and are prone to aneurysm formation. Aneurysm
dilatation, renal artery stenosis (renovascular HTA)
• Hypertensive (malignant) nephrosclerosis results in an "onion skin" appearance of the arterio
• Moderately increased albuminuria is the earliest manifestation of diabetic nephropathy. Early
administration of ACEi in patients with diabetes and moderately increased albuminuria can red
urinary albumin excretion and slow progression to vert DN.
• Systemic sclerosis damages connective tissue and small blood vessels thruough the body.
Scleroderma renal crisis is AKI and severe HTA. It is caused by immune mediated injury to sm
renal vessels that typically spares the glomerular capillaries (so there are no dysmorphic RBC o
RBC casts).

Pharmacology

• Urge incontinence treatment

○ Promote detrusor relaxation (B3 agonist)-Mirabegron. Few sistemic EA, very selective
○ Inhibiting contraction (antiM3 agonist)-Oxybutynin. Several EA, decreased cognition,
blurred vision
○ Vaptans (V2 antagonist) used to treat hyponatremia, no direct effect on NA+ or K+
excretion.
○ Metabolic alkalosis --> Loop diuretics
○ Ca inhibitors and K sparring diuretics: acidosis
§ Acetazolamide very usefull in metabolic alkalosis
§ Acetazolamide block reabsorption of sodium bicarbonate (NaHCO3)
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○ Vaptans (V2 antagonist) used to treat hyponatremia, no direct effect on NA+ or K+
excretion.
○ Metabolic alkalosis --> Loop diuretics
○ Ca inhibitors and K sparring diuretics: acidosis
§ Acetazolamide very usefull in metabolic alkalosis
§ Acetazolamide block reabsorption of sodium bicarbonate (NaHCO3)
○ All diuretics (except K sparring diruetics) -> hypokalemia
○ Sevelamer is used to control high blood levels of phosphorus in people with CKD, is a
nonabsorbable anion-exchange resin that binds intestinal phosphate to reduce absorptio
(decreases intestinal absorption of phosphorus).
○ Patiromer --> used to treat hyperkalemia, is a nonabsorbable cation exchange resin that
binds colonic potassium in exchange for calcium.
○ Common side-effects of ACEi include decreased GFR (increased creatinine) , hyperkalem
and cough. Most clinicians are generally not concerned by this unless the creatinine
increases by greater than 30%.
○ Aldosterone promotes K+ and H+ excretion and Na+ reabsorption
○ Beta adrenergic activity (cocaine, salbutamol) --> causes transient hypokalemia due to
increased transport of potassium intracellularly.
○ Aspirin toxicity --> altered mental status, elevated anion gap , tachypnea and hyperther
○ Anti-epileptic drug that induces ADH production and sensitivity -> Carbamazepine.
○ ACEi and ARB are the prefered antihyperteensive agents due to their antiproteinuric effe
in DM.
○ Post operatory urinary retention --> Bethanechol (muscarine agonist) or alfa 1 blocking
drug (tamsulosin)
○ Renal stenosis +ARB or iECA you must follow due to decreased GFR, RBP, FF
○ Mannitol increases plasma osmolality leading to the flow of water down its concentratin
gradient from the intracellular space to the plasma --> the resulting expansion also redu
serum sodium levels and increases glomerular filtration/tubular flow. Also glomerular
filtrate osmolality increases because mannitol is freely filtered and not reabsorberd.
○ Aldosterone secreting tumor. --> Primary hyperaldosteronism (Conn's syndrome) --> HT
hypokalemia, metabolic alkalosis, and decreased plasma renin activity. --> Tto is surgery
aldosterone antagonist (spironolactone or eplerenone)
§ Alternatively, hypoaldosteronism is the cause of type IV renal tubular acidosis.
○ Mannitol can cause pulmonary edema.
○ Loop and thiazide diuretics cause hypokalemia and metabolic alkalosis secondary to vol
contraction. You differentiate an intoxication of them with the calcium level
○ HTA with migraines --> Beta blocker due to its beneficial effect on migraine prophylaxis.
○ Calcitriol is the active form of VitD (1,25dihydroxyVItD)
○ Paracellular calcium reabsorption is couled to Na reabsorption, so if less Na is reabosrb
less Ca is reabsorbed.
○ Others:
○ Postoperative hypocalcemia is common after thyroid surgery, due to inadvertent remov
damage to the parathyroid glands. The acute drop in parathyroid hormone level result
decreased calcium and phosphate resorption from bone and decreased calcium
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 ○ Paracellular calcium reabsorption is couled to Na reabsorption, so if less Na is reabosrb
less Ca is reabsorbed.
○ Others:
○ Postoperative hypocalcemia is common after thyroid surgery, due to inadvertent remov
damage to the parathyroid glands. The acute drop in parathyroid hormone level result
decreased calcium and phosphate resorption from bone and decreased calcium
reabsorption by the kidneys.
○ Urine sodium<20 mEq/L csugest that initial oliguria is compensation for prerenal AKI.

• Lupus nephritis from systemic lupus erythematosus can manifest as

glomerulonephritis. Immunofluorescence microscopy showing a full house with 3
immunoglobulin classes (IgG, IgM, IgA) and 2 complement components (C3, C1q) is highly
characteristic.
○ patient's hematuria with proteinuria, renal insufficiency (elevated creatinine), and
sodium/fluid retention (hypertension and edema) are indicative of glomerulonephritis
(GN). Although GN has many etiologies, the patient's tender and swollen hand joints
(inflammatory arthritis) and renal biopsy findings are strongly suggestive of underlying
systemic lupus erythematosus.
• Vesicoureteral reflux typically occurs due to a congenitally shortened intravesical ureter leng
which prevents complete closure of the ureterovesical junction and allows retrograde urine
into the ureter during micturition. Most cases resolve spontaneously as the length of the
intravesical ureter increases with patient growth.
○ Posterior urethral valves occur due to abnormal development of the mesonephric
(Wolffian) duct. They can obstruct urine flow through the urethra; subsequent increase
intravesical pressure may cause reflux of urine into the ureter (ie, VUR). However, VUR
secondary to posterior urethral valves does not resolve spontaneously and almost
exclusively occurs in boys.
• The most common cause of urinary tract infection is Escherichia coli, a nitrate reductase–
producing bacterium. Dipstick analysis should be significant for leukocyte esterase, nitrites, an
mildly acidic pH.
○ Leukocyte esterase: Leukocyte esterase is an enzyme released by lysed white blood cell
and is a marker of inflammation. Although nonspecific, its presence is supportive of UTI
○ Nitrite: Nitrites are a metabolic by-product of bacteria producing nitrate reductase, an
enzyme that reduces normal urinary nitrate (NO3−) to nitrite (NO2−). These bacteria inclu
Escherichia coli and Proteus mirabilis. Enterococcus faecalis and Staphylococcus
saprophyticus do not produce nitrate reductase, making their presence inconsistent with
this patient's positive urinary nitrites (Choices B and F).
○ pH: Alkaline urine (pH >8) in the setting of UTI is suggestive of a bacterium that produce
urease (eg, Proteus mirabilis); urease hydrolyzes urea to ammonia (NH3), which is then
protonated to ammonium (NH4+), alkalizing the urine. This helps differentiate P mirabilis
from other nitrate reductase–producing bacteria. In this case, the patient has a relative
acidic (ie, pH = 5) urine, a finding that makes infection with P mirabilis unlikely
• Nephrotic syndrome in pored controlled rheumatoid arthritis is likely because of AA Amyloidos
in adults ( in children no abnormailty on light microscopy in nephrotic suggest minimal change
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 urease (eg, Proteus mirabilis); urease hydrolyzes urea to ammonia (NH3), which is then
protonated to ammonium (NH4+), alkalizing the urine. This helps differentiate P mirabilis
from other nitrate reductase–producing bacteria. In this case, the patient has a relative
acidic (ie, pH = 5) urine, a finding that makes infection with P mirabilis unlikely
• Nephrotic syndrome in pored controlled rheumatoid arthritis is likely because of AA Amyloidos
in adults ( in children no abnormailty on light microscopy in nephrotic suggest minimal change
disease)High ph In stoghorn calculus.
• Creatinine clearance overestimates GFR by 10-20% hand creatinine clearance has further
limitations
• Fever, maculopapular rash, and acute renal failure (elevated crestinine, oliguria) ocurring whit
feww weeks of starting a beta lactam antibiotic are highly sugestive of drug induced acute
interstitial nephritis (AIN). Many patients has increased levels of eosinophils in blood and urine
affects the renal interstitium. First thing in ATN is loss of epithelial cell polarity
• PFibroblat growth factor 23 is responsible to maintain serum phoshate levels in declining rena
function (FGF23 prevents hyperhposhatemia). FGF23 is secretd by osteoclast in response to
hyperphosphatemia, FGF23 suppresses 1 hydroxylase leading to reduce 1,25 hydroxyVItD (so l
intestinal phsphate absorption and renal reabsorption.
• Cystinuria has aminoaciduria
• Patients with chronic diarrhea or those who have had a colectomy have reduced bicarbonate
reabosrption from the gut, leading to state of chronic metabolic acidosis. Bichemical risck facto
of uric acid stone include low urine pH, low urine volume and hyperuricemia.
• A spontaneous kidney stone is usually due to normocalcemia and hypercacliuria (hypercalcem
may occur in prmari hyperparthiroidism, sarcodisis, malignancy and chronic acidemia).

• ACEi increase GFR (creatinine) initially, some EA include hyperkalemia and cough.

• HBP obstruction (and any chronic obstruction) leas to overflow incontinance. Over time, increa
urinary pressures can cause hydronephrosis and renal parenchymal atrophy with scarring. It ca
progress to CKD
• Ethylene glycol poisoning --> oxalate crystals. (ethylene glycol causes acute tubular necrosis w
vacuolar degeneration and ballooning of the proximal tubular cells).
• Manitol lowers serum sodium coconcentration because it moves water form de intercelluar sp
to the plasma. Manitol does not cross the BBB.
•
• antiHTA in diabetes --> ACEi
○ One of the earliest derangements that contributes to the pathognesis of diabetic
nephropatyh is an increase in the filtered glucose load. This increases sodium reasoropti
int the PTH leading yo decrease sodium delivery to the macula and subsequent activatio
the tubuloglomerular autoregulation sysyem. Subsequen dilatation of the afferent arteri
and constriction of the efferent arterioles increases intraglomerular capillary pressure,
resulting in an increase glomerular filtration rate.
• Brown casts suggest acute tubular necrosis. Ischemic kidney injury causes acute tubular necros
(ATN)predominantly affects the renal medulla, the most metabolically active segments pf the
nephorne are particulay vulenrable (proximal tubule and thick ascending limb --> outer medul
isquemia)
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 and constriction of the efferent arterioles increases intraglomerular capillary pressure,
resulting in an increase glomerular filtration rate.
• Brown casts suggest acute tubular necrosis. Ischemic kidney injury causes acute tubular necros
(ATN)predominantly affects the renal medulla, the most metabolically active segments pf the
nephorne are particulay vulenrable (proximal tubule and thick ascending limb --> outer medul
isquemia)
• Renal Faiulre: PTH elevated, serum calcium LOW, serum Phospurus Elevated, 25 hydroxyVitD
normal and 1,25 hydroxyVitD low.
• PAS stain to detect polysachaarides.
• PHPT is most pronounced in the cortical (compact) bone.
• High PTH lowers phosphate mainly lowers serum phosphate decreasing phosphate reabsorptio
proximal tubules.
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• Aspirin intoxication associate with tachypnea and hyperthermia
• Carbon monoxyde causes flu-like symptoms, headaches and altered
mental status.
• Above is the PCT
○ Creatinine is freely flitered in the kidney and no reabsorbed
○ Urea is freely filtered and poorly reabsorbed (reabsorption varies
throught the different tubular sysyems)
○ Rebsorption of sodium and potassim is approximately equal with
water
○ Bicarmonate is actively reaborbed
 ○ Creatinine is freely flitered in the kidney and no reabsorbed
○ Urea is freely filtered and poorly reabsorbed (reabsorption varies
throught the different tubular sysyems)
○ Rebsorption of sodium and potassim is approximately equal with
water
○ Bicarmonate is actively reaborbed
○ Glucosa and aa are avidly absorved

• The proximal tubules reabsorb more than 60% of the water filtered by
glomeruli regardless on the patient's hydration status.
• The proximal tubules reabsorb more than 60% of the water filtered by
glomeruli regardless on the patient's hydration status.

• If dehydrated, the lowest hypoosmolality is in the DCT.

• Renal cell carcinoma contains lots of lipid and glycogen:

• Secondary hyperaoldsteronism stimulates increased Na+ reabsorption as

well as a lesser degree of passive Cl- reabsorption (hypochloremia)

• ADH stimulates urea reabsorption in collecting ducts to maximize

corticopapillary osmotic gradient.
○ Vaptans are V2 antagonist used to treat hyponatremia. Vaptans
block ADH increasing renal free water excretion without directy
affectinh excretion of sodium or potassium

• Bethanechol is taken to treat certain disorders of the urinary

tract or bladder (it's a muscarinist agonist)

• Urge incontinence --> B3 adrenergic receptor agonist.

• Urge incontinence --> B3 adrenergic receptor agonist.

•
• Patients with multiple sclerosis develop a spastic bladder due to loss of
descending inhibitiory control from the upper motor neuron

• Isotonic saline solution can increase sodium levels. Also infusion of

• Isotonic saline solution can increase sodium levels. Also infusion of
excess normal saline can produce NAGMA (Non anion gap metabolic
acidosis). Increase sodium chloride can cause hypechloremia.
Hypechloremia can reduce the bicarbonate (CL- / HCO3- ) to maintain the
negayive balance.

• Endotelin 1 is a potent vasoconstrictor

• Diabetic ektoacidosis (like other metabolic acidosis ) is charactericed by

decrease serum pH and bicarbonate, elevated H2PO4- and
compensatory decrease in pCO2

• Renal cell carcinoma commonly arise from proximal tubule cells

• Patient with acute kidney injury, hyperkalemia and uranilysis 3+ blood

but no RBC has rhabdomyolysis, likely induced by prolonged seizure
(blod+ absecnseve of RBC sugest on uranalysis myoglobinuria). Heme
pgiemnt of myoglobin causes acute tubular necrosis by citotoxicity and
vasoconcstrictino
• Smoking is one of the most importatn risk factors for renal cell cacrinoma

• Penicillamine can present with neprohotic syndrome due to

membranous nephropathy

• AINES can cause minimal change disease (most common cause of

nephritic in children). In adults AINES causes mostly membranous
nephropaty.

• Cystinuria:

• Prolonged use of EPO can lead to thromboembolism and hypertension.

 • Prolonged use of EPO can lead to thromboembolism and hypertension.

• Beta blockers:
○ BLOCK RENIN RELEASE
○ Block sympathetic stim of JG apparatus

• Metabolic alkalosis in fluid loss (vomiting or GI losses )

○ Urine chloride is useful determining the cause of the acid base
distrubance (low sugest vomiting)

• Urinary chloride is low in surreptitious vomiting

• Patent urachus presents with straw-colored urine discharge from the

• Patent urachus presents with straw-colored urine discharge from the
umbilicus, which is exacerbated by cryung, straining or prone position.