Steve O's Ridiculous Renal Realities Flashcards
(127 cards)
1
Q
Mesonephros
A
functions as the interim kidney for 1st trimester;
later contributes to the male genital system
2
Q
Metanephros
A
permanent;
first appears in 5th week of gestation;
nephrogenesis continues through 32-26 weeks of gestation;
Contains ureteric bud, metanephric mesenchyme,
3
Q
Ureteric bud
A
derived from caudal end of mesonephric duct;
gives rise to ureter, pelvises, calyces, and collecting ducts;
fully canalized by 10th week
4
Q
metanephric mesenchyme
A
ureteric bud interacts with this tissue;
interaction induces differentiation and formation of glomerulus through the distal convoluted tubule
5
Q
Ureteropelvic junction
A
last to canalize and the most common site of obstruction (hydronephrosis) in fetus
6
Q
Potter’s sequence
A
Oligohydramnios causing compression of developing fetus leading to limb deformities, facial anomalies (low set ears, and retrognathia) and and compression of chest leading to pulmonary hypoplasia (cause of death);
causes include ARPKD, posterior urethral valves, bilateral renal agenesis
7
Q
Horseshoe kidney
A
Inferior poles of both kidneys fuse;
as they ascend from pelvis, get trapped under inferior mesenteric artery and remain low in the abdomen;
kidney function is normal;
increased risk for ureteropelvic junction obstruction, hydronephrosis, renal stones, and rarely renal cancer (wilms tumor);
associated with Turner Syndrome
8
Q
Multicystic dysplastic kidney
A
Due to abnormal interaction between ureteric bud and metanephric mesenchyme;
this leads to a nonfunctional kidney consisting of cysts and connective tissue;
if unilateral (most common), generally asymptomatic with compensatory hypertrophy of contralateral kidney;
often diagnosed prenatally via ultrasound;
not inherited, cysts are in renal parenchyma
9
Q
Why is the left kidney taken during living donor transplant?
A
Because the renal vein is longer
10
Q
Ureters: what is the course from kidney to bladder
A
pass under uterine artery and under ductus deferens (retroperitoneal);
Water under bridges;
Gynecologic procedures involving ligation of the uterine vessels may damage the ureter leading to ureteral obstruction or ureteral leak
11
Q
Glomerular filtration barrier
A
Filters based on charge and on size;
Composed of- Fenestrated capillary endothelium (size barrier), Fused basement membrane with heparan sulfate (negatively charged barrier), Epithelial layer consisting of podocyte foot processes;
12
Q
When is the charge barrier lost in the GF barrier
A
Lost in nephrotic syndrome, resulting in albuminuria, hypoproteinemia, generalized edema, and hyperlipidemia
13
Q
How to measure effective renal plasma flow
A
estimated using para-aminohuppuric acid (PAH) clearance because it is both filtered and actively secreted in the proximal tubule;
nearly all PAH entering the kidney is excreted
14
Q
Glucose clearance
A
Glucose reabsorbed in PCT;
anything over ~200 not reabsorbed;
15
Q
Amino acid clearance
A
Sodium dependent transporters in proximal tubule reabsorb amino acids;
16
Q
Hartnup disease
A
autosomal recessive;
deficiency of neutral amino acid (e.g. tryptophan) transporters in proximal renal tubular cells and on enterocytes;
leads to neutral aminoaciduria and decreased absorption from the gut;
results in pellagra like symptoms;
treat with high protein diet and nicotinic acid
17
Q
Fluid compartments and their size
A
60% is total body water;
40% total body weight is intracellular;
20% of total body weight is extracellular;
5% of total body weight is plasma volume;
15% of total body weight is interstitial volume
18
Q
Notable components of PCT
A
contains brush border;
reabsorbs all glucose and amino acids and most of the bicarb, Na, Cl, Phosphate, K+, and H2O;
isotonic absorption;
generates and secretes NH3, which acts as a buffer for secreted H+;
PTH inhibits Na/Phosphate cotransport leading to secretion of Phosphate;
ATII stimulates Na/H+ exchange causing increased Na, H2O, and bicard reabsorption (permitting contraction alkalosis);
65-80% Na reabsorbed here
19
Q
Thin descending loop of henle
A
Passively reabsorbs H2O via medullary hypertonicity (impermeable to Na+);
concentrating segment;
Makes urine hypertonic
20
Q
Important components of the Loop of Henle
A
Actively reabsorbs Na, K, and Cl-;
indirectly induces the parallel reabsorption of Mg2+ and Ca2+ through + lumen potential generated by K+ backleak;
impermeable to H20;
makes urine less concentrated as it ascends;
10-20% Na reabsorbed
21
Q
important components of the Distal Convoluted Tubule
A
Actively reabsorbs Na and Cl;
makes urine hypotonic;
PTH increases Ca/Na exchange leading to Ca reabsorption;
5-10% of Na reabsorbed
22
Q
Important components of the collecting tubule
A
Reabsorbs Na in exchange for secreting K and H (regulated by aldosterone);
aldosterone acts on mineralcorticoid receptor which inserts Na channel on luminal side;
ADH acts on V2 receptor inserting aquaporin channel;
3-5% Na reabsorbed here
23
Q
Fanconi syndrome
A
Reabsorptive defect in PCT;
assoc. w/ increased excretion of nearly all amino acids, glucose, bicarb, and phosphate;
may result in metabolic acidosis (proximal renal tubular acidosis);
causes include hereditary defects (e.g. wilson disease), ischemia, and nephrotoxins/drugs;
FABulous Glittering Liquid
24
Q
Bartter syndrome
A
Reabsorptive defect in thick ascending loop of henle;
autosomal recessive, affects Na/K/2Cl cotransporter;
results in hypokalemia, and metabolic alkalosis with hypercalciuria;
FABulous Glittering Liquid
25
Gitelman syndrome
```
Reabsorptive defect of NaCl in DCT;
Autosomal recessive;
less severe than Bartter syndrome;
leads to hypokalemia and metabolic alkalosis, but no hypercalciuria;
FABulous Glittering Liquid
```
26
Liddle syndrome
Increased Na reabsorption in distal and collecting tubules (increased activity of epithelial Na channel);
autosomal dominant;
results in HTN, hypokalemia, metabolic alkalosis, decreased aldosterone;
treat with amiloride
27
Where does Angiotensin II go to have an effect
1) acts on AT I receptors on smooth muscle causing vasoconstriction and increased BP;
2) constricts efferent arteriole causing increased FF to preserve GFR in low volume states;
3) activates aldosterone;
4) activates ADH release from posterior pituitary;
5) Stimulates hypothalamus causing thirst
28
ANP
released from atria in response to increased volume;
may act as a check on RAAS;
relaxes smooth muscle via cGMP causing increased GFR and decreased renin
29
ADH: what does it respond to
primarily regulates osmolarity;
| also responds to low blood volume
30
Aldosterone: what does it regulate
Primarily regulates ECF Na+ content and volume;
| responds to low blood volume states as well
31
Juxtaglomerular apparatus
consists of JG cells (modified smooth muscle of afferent arteriole) and the macula densa (NaCl sensor, part of the distal convoluted);
JG cells secrete renin in response to decreased renal blood pressure, decreased NaCl deliver to distal tubule and increased sympathetic tone (B1);
note that beta blockers work here as well as heart
32
Erythropoietin
released by interstitial cells in the peritubular capillary bed in response to hypoxia;
33
Kidney function on Vit. D
Proximal tubule cells convert 25-OH vit. D to 1,25-(OH)2 vitamin D;
Via 1alpha-hydroxylase (increased by PTH)
34
Renin secreted by
JG cells in response to decreased renal arterial pressure and increased renal sympathetic discharge via beta1
35
Prostaglandins and their effect on kidneys
Paracrine secretion vasodilates the afferent arterioles to increase RBF;
NSAIDs block this leading to constriction of the afferent arteriole and decreased GFR;
this may result in acute renal failure
36
Potassium shift due to digitalis
K shift out of cells
37
Potassium shift due to hyperosmolarity
K+ shifts out of cell
38
Potassium shift due to hypo-osmolarity
K+ shifts into cell
39
Potassium shift due to insulin deficiency
K+ shifts out of cell
40
Potassium shift due to insulin activity
K+ shifts into cell (increased Na/K ATPase)
41
Potassium shift due to lysis of cells
K+ shifts out of cell
42
Potassium shift due to acidosis
K+ shifts out of cell
43
Potassium shift due to alkalosis
K+ shifts into cell
44
Potassium shift due to beta adrenergic antagonist
K+ shifts out of cell
45
Potassium shift due to beta adrenergic agonist
K+ shifts into cell (increased Na/K ATPase)
46
Symptoms of low Na level
Nausea, malaise, stupor, coma
47
symptoms of high Na level
Irritability, stupor, coma
48
Symptoms of Low K level
U wave on ECG, flattened t waves, arrhythmias;
| muscle weakness
49
Symptoms of High K level
Wide QRS and peaked T waves on ECG, arrhythmias;
| muscle weakness
50
Symptoms of low Ca2+ levels
Tetany, seizure, QT prolongation
51
Symptoms of high Ca2+ levels
stones (renal), bones (pain), groans (abdominal pain), psychiatric overtones (anxiety, altered mental status), but not necessarily calciuria
52
Symptoms of low Mg2+ levels
tetany, torsades de pointes
53
Symptoms of high Mg2+ levels
Decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
54
Metabolic Acidosis with increased anion gap (>12)
MUDPILES;
| Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron or INH, Lactic acidosis, Ethylene glycol, Salicylates
55
Metabolic acidosis with normal anion gap (8-12)
HARDASS;
| Hyperalimentation, Addison disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spironolactone, Saline infusion
56
Renal tubular acidosis in general
a disorder of the renal tubules which leads to non-anion gap hyperchloremic metabolic acidosis
57
Renal tubular acidosis: type 1
Distal, pH >5.5;
Defect in ability of alpha intercalated cells to secrete H+, thus new bicarb is not generate leading to metabolic acidosis;
associated with hypokalemia, increased risk for calcium phosphate kidney stones (due to increased pH and increased bone turnover);
Caused by amphotericin B toxicity, analgesic nephropathy, multiple myeloma (light chains), and congenital anomalies (obstruction) of the urinary tract
58
Renal tubular acidosis: type 2
Proximal, pH
59
Renal tubular acidosis: Type 4
Hyperkalemic, pH
60
What are the causes of RBC casts
glomerulonephritis, ischemia, or malignant HTN;
61
What are the causes of WBC casts
tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
62
What are the causes of Fatty casts
oval fat bodies;
| nephrotic syndrome
63
What are the causes of Granular casts
muddy casts;
| Acute tubular necrosis
64
What are the causes of Waxy casts
advanced renal disease/chronic renal failure
65
What are the causes of hyaline casts
Nonspecific, can be a normal finding, often seen in concentrated urine samples
66
Nomenclature for glomerular disorders: Focal
67
Nomenclature for glomerular disorders: diffuse
>50% of glomeruli are involved;
| e.g. diffuse proliferative glomerulonephritis
68
Nomenclature for glomerular disorders: Proliferative
Hypercellular glomeruli;
| e.g. Mesangial proliferation
69
Nomenclature for glomerular disorders: membranous
thickening of glomerular basement membrane;
| e.g. membranous nephropathy
70
Nomenclature for glomerular disorders: primary glomerular disease
Involve only glomeruli;
this a primary disease of the kidney;
e.g. minimal change disease
71
Nomenclature for glomerular disorders: Secondary glomerular disease
Involves glomeruli and other organs, this a disaese of another organ system, or a systemic disease that has impact on the kidney;
e.g. SLE, diabetic nephropathy
72
Glomerular diseases that cause Nephritic syndrome
Berger (IgA glomerulonephropathy);
Acute Poststreptococcal glomerulonephritis;
Alport syndrome;
Rapidly progressive glomerulonephritis
73
Glomerular diseases that cause Nephrotic syndrome
```
Focal segmental glomerulosclerosis;
Membranous nephropathy;
Minimal change disease;
amyloidosis;
Diabetic glomerulonephropathy
```
74
Glomerular diseases that cause both nephritic and nephrotic
Diffuse proliferative glomerulonephritis;
| membranoproliferative glomerulonphritis
75
Nephrotic syndromes in general cause what
nephrOtic syndrome presents with massive prOteinuria (>3.5 g/day, forthy urine), hyperlipidemia, fatty casts, edema;
Assoc. w/ thromboembolism (hypercoagulable state due to AT III loss in urine);
increased risk of infection (loss of immunoglobulins)
76
Focal segmental glomerulosclerosis
LM-segmental sclerosis and hyalinosis;
IF is negative;
EM effacement of foot process similar to minimal change disease;
Most common cause of nephrotic syndrome in blacks and hispanics;
can be assoc. w/ HIV, sickle cell, interferon treatment, and chronic kidney disease due to congenital absence or removal;
inconsistent response to steroid therapy;
may progress to chronic renal disease
77
Membranous nephropathy
LM- diffuse capillary and GBM thickening;
IF-Granular as a result of immune complex deposition;
EM- Spike and Dome with subepithelial deposits;
most common cause of primary nephrotic syndrome in whites;
can be associated with antibodies to phopholipase A2 receptor, drugs (NSAIDs, penicillamine), infections, SLE or solid tumors;
poor response to steroids;
may progress to chronic renal disease;
78
Minimal change disease
LM-normal glomeruli (lipid may be present in PCT cells);
IF is negative;
EM will show effacement of the foot processes;
Nephrotic syndome;
Most common in children;
may be triggered by recent infection, immunization, or immune stimulus;
may be assoc. w/ hodgkin lymphoma (e.g. cytokine mediated damage);
excellent response to corticosteroids
79
Amyloidosis Nephrotic syndome
LM- congo red stain shows apple-green birefringence under polarized light;
kidney is the most commonly involved organ;
assoc. with chronic conditions (e.g. Multiple Myeloma, TB, rheumatoid arthritis)
80
Membranoproliferative glomerulonephritis
nephritic syndrome that can also present as Nephrotic;
Type 1- subendothelial immune complex deposition with granular IF;
tram track appearance due to GBM splitting caused by mesangial ingrowth;
Associated with HBV, HCV, may be idiopathic
Type 2- Intramembranous IC deposits "dense deposits";
associated with C3 nephritic factor (stabilizes C3 convertase leading to decreased serum C3 levels
81
Diabetic glomerulonephropathy
LM- mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (kimmelstiel Wilson lesion);
nonenzymatic glycosylation of efferent arterioles leading to increased GFR and increased mesangial expansion
82
Overview of nephritic syndromes
nephrItic=Inflammatory;
when it involves glomeruli it leads to hematuria and RBC casts in urine;
associated with azotemia, oliguria, HTN (due to salt retention), and proteinuria (
83
Acute poststreptococcal glomerulonephritis
LM-glomeruli enlarged and hypercellular;
IF- (starry sky) granular appearance (lumpy bumpy) due to IgG, IgM, and C3 deposition along GBM and mesangium;
EM- subepithelial immune complex (IC) humps;
Most frequently in children;
occurs ~2 weeks after group A strep infection of pharynx, skin;
resolves spontaneously;
Type III hypersensitivity;
presents with peripheral and periorbital edema, dark urine (cola colored), and HTN;
increased anti-DNase B titers and decreased compliment levels
84
Rapidly progressing glomerulonephritis
Can present as nephritic or nephrotic;
LM and IF show crescent moon shape;
crescents consist of fibrin and plasma protein (e.g. C3b) w/ glomerular parietal cells, monocytes, and macrophages;
Associated with goodpastures, granulomatosis w/ polyangitis, microscopic polyangiitis;
Poor prognosis;
rapidly deteriorating renal function (Days to weeks)
85
Goodpasture syndrome
type II hypersensitivity;
antibodies to GBM and alveolar basement membrane causing linear IF;
Hematuria/hemoptysis;
against type IV collagen (lungs, kidney, and lens)
86
Diffuse proliferative glomerulonephritis
```
due to SLE or MPGN;
LM "loop wiring" of capillaries;
EM- subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition;
IF- granular;
Most common cause of death in SLE;
can be nephritic or nephrotic
```
87
IgA nephropathy
```
AKA berger disease;
Nephritic syndrome;
LM- mesangial proliferation;
EM- mesangial IC deposits;
IF- IgA based IC deposits in mesangium;
seen in HSP;
often presents/flares with a URI or acute gastroenteritis;
episodic hematuria with RBC casts
```
88
Alport syndrome
presents as nephritic syndrome;
Mutation in type IV collagen leading to thinning and splitting of the glomerular basement membrane;
Most commonly X-linked;
Glomerulonephritis, deafness, and less commonly eye problems
89
Urine dipstick is positive for RBCs in urine, what does this mean
means dipstick reacted to peroxidase reaction of hemoglobin;
if no RBCs seen under microscopy then you have myoglobinurea;
myoglobinurea will cause reactive oxygen species so hydrate and alkalination of urine must be done
90
Calcium renal stones
See envelope or dumbbell shaped crystals in urine;
radiopaque;
precipitates in increased pH (calcium phosphate) and decrease pH (calcium oxylate);
Promoted by hypercalciuria (look for diseases that increase Ca levels);
oxalate crystals can come from ethylene glycol (antifreeze), vit C abuse, Crohn disease;
prevent with Thiazide, citrate, and increased fluid;
Most common stone is calcium oxylate
91
Ammonium Magnesium Phosphate renal stones
Coffin lid crystals;
Radiopaque;
precipitate at increased pH;
AKA struvite stone;
caused by infection (urease + like proteus, kleb, staph);
can form staghorn calculi that can be nidus for UTIs;
treat with eradication of underlying infection and surgical removal of stone
92
Uric Acid renal stones
Rhomboid or rosettes stone;
radiolucent;
precipitate at decreased pH;
Risk factors- decreased urine volume, arid climates, and acidic pH;
visible on CT and ultrasound, not on x-ray;
strong association with hyperuricemia (like gout);
often seen in leukemia (high cell turnover diseases);
treat with alkalization of urine
93
Cystine renal stones
Hexagonal stones;
radiopaque;
precipitate in decreased pH;
mostly seen in children, secondary to cystinuria;
can form staghorn calculi;
sodium nitroprusside test +;
treat with alkalinization of urine and increased hydration
94
Hydronephrosis
distention/dilation of the renal pelvis and calyces;
usually caused by urinary tract obstruction;
other causes include retroperitoneal fibrosis and vesicoureteral reflux;
dilation occurs proximal to site of pathology;
only impairs renal function if bilateral or patient only has one kidney;
leads to compression atrophy of renal cortex and medulla
95
Renal cell carcinoma
originates from proximal tubule cells;
see polygonal clear cells filled with accumulated lipids and carbohydrates;
most common in men 50-70;
increased incidence in smokers and obesity;
manifests clinically with hematuria, palpable mass, secondary polycythemia, flank pain, fever, and weight loss, invades renal vein then IVC and spreads hematogenously;
metastasizes to lung and bone;
associated with defect in chromosome 3 (von-hippel-lindau);
resistant to chemo and radiation;
most common primary renal malignancy
96
Renal oncocytoma
Benign epithelial cell tumor;
large eosinophilic cells with abundant mitochondria without perinuclear clearing (vs. chromophobe RCC);
presents with painless hematuria, flank pain, and abdominal mass;
treat with nephrectomy
97
Wilms tumor
nephroblastoma;
most common renal malignancy of early childhood (ages 2-4);
contains embryonic glomerular structures;
presents with huge, palpable flank mass and/or hematuria;
Loss of function mutations in tumor suppressor genes WT1 or WT2 on chromosome 11;
may be part of beckwith-Wiedemann syndrome or WAGR complex (Wilms, Aniridia, Genitourinary malformation, mental Retardation)
98
Transitional Cell Carcinoma
Most common tumor of urinary tract system;
can occur in renal pelvis, renal calyces, ureters, and bladder;
painless hematuria (no casts) suggests bladder cancer;
associated with problems in your Pee SAC (Phenacetin, Smoking, Aniline dyes, and Cyclophosphamide)
99
Squamous cell carcinoma of the bladder
Chronic irritation of urinary bladder leads to squamous metaplasia causing dysplasia and squamous cell carcinoma;
Risk factors include Schistosoma haematobium infection (middle east), chronic cystitis, smoking, chronic nephrolithiasis;
presents as painless hematuria
100
Acute infectious cystitis
inflammation of urinary bladder;
presents as suprapubic pain, dysuria, urinary frequency, and urgency;
systemic signs (fever, chills) are usually absent;
Risk factors include female, sexual intercourse, and indwelling catheters;
causes- e coli, staph saprophyticus, klebsiella, proteus mirabilis (ammonia scent), adenovirus (hemorrhagic cystitis);
Lab findings- + leukocyte esterase, nitrites appear for gram - organisms, sterile pyuria and - urine cultures suggests gonorrhoeae or chlamydia
101
Acute pyelonephritis
Affects cortex w/ sparing of glomeruli and vessels;
presents with dysuria, fever, CVA tenderness, nausea, and vomiting;
caused by ascending UTI (e coli), vesiculoureteral reflux, and hematogenous spread to kidney;
often presents with WBC casts in urine;
CT shows striated parenchymal enhancement;
risk factors are indwelling urinary catheter, tract obstruction, DM, and pregnancy;
Complications include chronic pyelonephritis, renal papillary necrosis, perinephric abscess;
treat with antibiotics
102
Chronic pyelonephritis
the result of recurrent episodes of acute pyelonephritis;
typically requires predisposition to infection such as vesicoureteral reflux or chronic obstructing kidney stones;
Coarse asymmetric corticomedullary scarring, blunted calyx;
tubules can contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney)
103
Drug-induced interstitial nephritis (tubulointerstitial nephritis)
Acute interstitial renal inflammation;
pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as haptens, inducing hypersensitivity;
nephritis typically occurs 1-2 weeks after certain drugs (e.g. diuretics, penicillin derivatives, sulfonamides, rifampin), but can occur months after starting NSAIDs;
associated with fever, rash, hematuria, and CVA tenderness, but can be asymptomatic
104
Diffuse cortical necrosis
Acute generalized cortical infarction of both kidneys;
likely due to a combination of vasospasm and DIC;
associated with obstetric catastrophes (e.g. abruptio placentae) and septic shock
105
Avute tubular necrosis: stages and overview
most common cause of intrinsic renal failure;
self-reversible in some cases, but can be fatal if not treated;
death most often occurs during initial oliguric phase;
findings- granular (muddy brown) casts;
3 stages- 1) inciting event 2) maintenance phase-oliguric, lasts 1-3 weeks, risk of hyperkalemia, metabolic acidosis 3) recovery phase-polyuric, BUN and creatinine fall, risk of hypokalemia
106
Avute tubular necrosis: 2 types
1) Ischemic- secondary to decreased renal blood flow (e.g. hypotension, shock, sepsis, CHF), results in death of tubular cells that may slough into tubular lumen (proximal tubule and thick ascending limb are highly susceptible to injury)
2) Nephrotoxic- secondary to injury resulting from toxic substances (e.g. aminoglycosides, radiocontrast agents, lead, cisplatin), crush injury (myoglobinurea), hemoglobinuria, proximal tubule is particularly susceptible to injury
107
Renal papillary necrosis
Sloughing of renal papillae leading to gross hematuria and proteinuria;
may be triggered by a recent infection or immune stimulus;
associated with DM, acute pyelonephritis, chronic phenacetin use (acetaminophen is phenacetin derivative), sickle cell anemia and trait
108
Acute Renal Failure
In normal nephron BUN is reabsorbed (for countercurrent multiplication), but creatinine is not;
acute kidney injury is defined as an abrupt decline in renal function with increased creatinine and increased BUN over a period of several days
109
Prerenal azotemia
As a result of decreased RBF (e.g. hypotension) causing decreased GFR;
Na/H2O and urea retained by kidney in an attempt to conserve volume, so BUN/creatinine ratio increases;
urine osmolarity > 500;
urine Na 20
110
Intrinsic renal failure
Generally due to acute tubular necrosis or ischemia/toxins;
less commonly due to acute glomerulonephritis (e.g. RPGN);
patchy necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule leading to decreased GFR;
urine has epithelial/granular casts;
BUN reabsorption is impaired leading to decreased BUN/creatinine ratio;
Urine osmolarity 40;
FENa >2%;
Serum BUN/Cr
111
Postrenal azotemia
due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies);
develops only with bilateral obstruction;
Urine osmolarity 40;
FENa >1% (mild)-2% (if severe);
Serum BUN/Cr >15
112
Consequences of renal failure
inability to make urine and excrete nitrogenous waste;
MAD HUNGER- Metabolic Acidosis, Dyslipidemia (increased tg), Hyperkalemia, Uremia (increased bun and creatinine), Na/h2o retention, Growth retardation, Erythropoietin failure (anemia), Renal osteodystrophy
113
Renal osteodystrophy
Failure of Vit D hydroxylation, hypocalcemia, and hyperphosphatemia leading to secondary hyperparathyroidism;
hyperphosphatemia also independently decreased serum Ca by causing tissue calcifications, whereas decreased 1,25-(OH)2 vitamin D leads to decreased intestinal Ca2+ absorption;
causes subperiosteal thinning of bones
114
ADPKD
adults;
bilateral enlarged kidneys with tons of cysts;
destroys the kidney parenchyma;
presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure;
Autosomal dominant defect in PKD1 (85%, chromosome 16) or PKD2 (15%, chromosome 4);
death from chronic kidney disease or HTN (caused by increased renin);
associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts
115
ARPKD
Infants;
autosomal recessive;
associated with congenital hepatic fibrosis;
significant in utero renal failure can lead to potter sequence;
future concerns of HTN, portal HTN, progressive renal insufficiency;
no surface cysts like ADPKD, only in parenchyma
116
medullary cystic disease
Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine;
medullary cysts usually not visualized;
shrunken kidneys on ultrasound;
poor prognosis
117
simple vs complex renal cyst
simple cysts usually found in outer cortex filled with ultrafiltrate, very common, and account for majority of all renal masses, found incidentally and typically asymptomatic;
Complex cysts, including those that are septated, enhanced, or have solid components as seen on CT, require follow-up or removal due to risk of renal cell carcinoma
118
Mannitol
osmotic diuretic, increased tubular fluid osmolarity, producing increased renal flow, decreased ICP and Intraocular pressure;
used for drug overdose, increased intracranial/ocular pressure;
toxicity-pulmonary edema, dehydration;
contraindicated in anuria, CHF
119
Acetazolamide
mechanism- carbonic anhydrase inhibitor, causes self-limited sodium bicarb diuresis and decreased total body bicarb stores;
used for glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri;
toxicity-hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy
120
Furosemide
Mechanism: inhibits Na/K/2Cl of thick ascending limb of loop Henle, abolishes hypertonicity of medulla, preventing concentration of urine, stimulates PGE release (vasodilate afferent arteriole), increased Ca excretion (loops loose Ca);
used for edema, HTN, and hypercalcemia;
toxicity- ototoxicity, hypokalemia, dehydration, allergy (sulfa), Nephritis (interstitial), Gout, OH DANG!
121
Ethacrynic acid
Mechanism- phenoxyacetic acid derivative (not a sulfonamide), essentially same action as furosemide;
Use: diuresis in patients allergic to sulfa drugs;
Toxicity: same as furosemide, can cause hyperuricemia, never use to treat gout
122
Hydrochlorothiazide
inhibits NaCl reabsorption in early distal tubule, decreasing diluting capacity of the nephron, decreased Ca excretion (increasing plasma Ca, so if increased PTH don't give);
Uses- HTN, CHF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, osteoporosis;
toxicity- hypokalemic metabolic acidosis, hyponatremia, hyperglycenmia, hyperlipidemia, hyperuricemia, and hypercalcemia, sulfa drug
123
K+ sparing diuretics:
Spironolactone and eplerenone are competitive aldosterone receptor antagonists in the cortical collecting tubule;
triamterene and amiloride act at the same part of the tubule by blocking Na channels in CCT;
uses- hyperaldosteronism, K depletion, CHF;
Toxicity- hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (gynecomastia, antiandrogen effects)
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ACE inhibitors: mechanism
captopril, enalapril, lisinopril;
inhibit ACE, decreasing ATII causing decreased GFR by preventing constriction of efferent arterioles;
levels of renin increase as result of loss of feedback inhibition;
inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator;
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ACE inhibitors: uses
captopril, enalapril, lisinopril;
| HTN, CHF, proteinuria, diabetic nephropathy, prevent unfavorable heart remodeling as a result of chronic HTN;
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ACE inhibitors: toxicity
CATCHH;
Cough, Angioedema (contraindicated in Cl esterase inhibitor deficiency), Teratogenic (fetal renal malformations), increased Creatinine (decreased GFR), Hyperkalemia, and Hypotension;
avoid in bilateral renal artery stenosis because it will cause further GFR decrease
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Angiotensin II receptor blockers
ARBS;
-sartans;
similar to ACE inhibitors but do not increased bradykinin so less chance of cough;
Competitively inhibits ATII at angiotensin I receptor;
AT II is the most powerful Na retention hormone
