Renal: General Flashcards
GPA ass renal finding
Pauci-immune crescentic glomerulonephritis
Muddy brown granular casts indicate
Acute tubular necrosis
- rash,
- fever and
- eosinophilia
urine sediment, if present, = WBC (and/or red cell) casts/pyuria.
interstitial nephritis
Bartter’s syndrome
- What is defective & where
-inheritance
- Results
-What drug acts like this
Bartter’s syndrome
AR
- defective Cl- absorption at the Na+ K+ 2Cl- cotransporter (NKCC2)
- ascending loop of Henle
HYPO K -normotension-
metabolic alkalosis
Where do Loop work
MOA
Examples
SE
Ascending Loop of Henle
Na/K cotransporter blked
- ide-Bumetanide , Ethacrynic acid,
Furosemide ,Torsemide
-HypoNa & HypoK
Gitelman syndrome
- What is defective & where
-inheritance
- Results
-What drug acts like this
Defect NaCL cotransporter in the DCT
-AR
HypoK + Norm tension
metabolic ALKalosis.
hypocalciuria/ hyperCa2+
Thiazides - HyperGluc
Causes of Hypok with htn
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Liddle’s syndrome
11-beta hydroxylase deficiency*
Hypokalaemia without hypertension
- diuretics
- GI loss (e.g. Diarrhoea, vomiting)
renal tubular acidosis (type 1 and 2**) - Bartter’s syndrome
- Gitelman syndrome
What does HyperGLUC stand for
Hyper: Glucose, Lipids, Uremia, Ca2
SE of thiazides
SE thiazides
And site of action
Hyper: Glucose, Lipids, Uremia, Ca2
HypoK + metabolic ALKalosis
-DCT
NaCl cotransporter
Liddle syndrome
- What is defective & where
-inheritance
- Results
-What drug acts like this
- Collecting ducts
-AD - Hypo K with HTN & Metabolic alkalosis
Fanconi Syn
where does it effect
Hereditary causes
Acquired
Drug
-PCT defect
Causes
- Hereditary: Wilsons, tyrosinemia, Glycogen storage disorders
- Acquired: Ischemia, MM
- Drug :Cisplatin, expired tetracyclines, Ifsofamine
Where do N/K transporter work
Ascending loop of Henle
(Defect batters)
Where do Nacl cotransporters work
DCT
(Gitelmen syn)
What is reabsorbed in PCT
( nep–>cir)
Lipids
Small proteins
HCO3-
H2O
Glucose -100%
Na- 65%
K- 60%
CL- 60%
Urea -50%
What is reabsorbed in DLOH
H20
What is reabsorbed in thick ascending loop of Henle
Defect and drugs
reabsorbs K, Cl & Na
via Na/K/Cl, cotransporter or NKCC2,
Bartter’s
Loops
What is reabsorbed in DCT
Defect
Drug
reabsorbs Na, Cl-, Via a Na -Cl cotransporter,
as well as Ca2+ & mg.
- Gitelman
- Thiazide
Causes Respiratory acidosis (4)
Hypoventilation
- decompensation resp d e.g. life-threatening asthma / pulmonary oedema
- neuromuscular disease
- obesity hypoventilation syndrome
- sedative drugs: benzodiazepines, opiate overdose
Causes Respiratory Alkalosis (4)
Hyperventilation
due to hyperventilation
- normal pregnancy
- hysteria
- hypoxemia (e.g., high altitude)
- salicylates (early)
- PE
- pneumonia
CNS disorders: stroke, SAH, encephalitis
normal anion gap metabolic acidosis
(Normal Hardass)
Hyperalimentation
Addison’s disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
mnemonic: HARDASS
Elevated anion gap metabolic acidosis
(elevated mudpiles )
Methanol (formic acid)
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets or isoniazid
Lactic acidosis (such as by metformin toxicity)
Ethylene glycol
Salicylates (late)
mnemonic: MUDPILES
PH
HCO3/CO2
Explain metabolic Acidosis with resp compensation
Is this what you expect to happen to this PH:
Low PH = acidosis
HCO3 (metabolic) is proportional to PH thus if decreased = met acid
CO2 (respiratory) is inversely proportional you would expect a rise; if it isn’t then compensation.
PH always matches the primary defect
Lab in Pre renal AKI
GFR
Urea
Na and urine osmolality
Pre renal
Decrease bl. Flow = decrease GFR
less urea and creatinine are filtered out, and more stays in the blood, so levels of BUN and creatinine will be high.
aldosterone (low bp)= reabsorb sodium= Na reabsorption is also tied to urea reabsorption, = urea gets reabsorbed and so even more urea gets into the blood = > 20:1 creat
Na is retained, = urine Na is < 20 mEq/L
urine is more concentrated (less water excreted) urine’s > 500 milliosmoles per kilogram.
Causes of Pre renal AKI
-Hypovolemic (hemorrhage, D&V diuretics)
- Hypervolemic states where there’s a low effective circulating volume. sHF (cardiorenal syndrome).
-systemic vasodilation, (sepsis)
Lab in Inter renal AKI
GFR
Urea
Na and urine osmolality
Hindered reabsorption
Urea isn’t reabsorbed = less urea stays in the blood relative to creatinine, and the BUN: creatinine ratio < 20:1
NA NOT reabsorb =urine Na+ >40 mEq/L
H20 not reabsorbed = urine osmolality falls below 350 mOsm/kg.
Causes of inter-renal AKI
-damage to the tubules, the glomerulus, or the kidney interstitium (4)
- Mainly ATN (prolonged ischemia & Nephrotoxins )
- acute interstitial nephritis
- infections -Mycoplasma
- autoimmune conditions,
Sjogren syndrome, sarcoidosis or SLE - acute glomerulonephritis
- HUS
- diffuse cortical necrosis -Combination of vasospasm & DIC
- renal papillary necrosis- ass. SS
Drug causes of Renal AKI ATN (7)
1.contrast dyes,
2. aminoglycosides
3. cisplatin,
4. heavy metals like lead,
5. myoglobin (rhabdomyolysis),
6. ethylene glycol
7. radiocontrast dye, and hemoglobinuria
Think: Heave metal signer drinking ethylene glycol
Causes of acute interstitial nephritis (5)
type I or type IV hypersensitivity
1. NSAIDs(analgesic nephropathy)
2.penicillin,
3. Rifampin,
4. PPI’sand
5. Diuretics
Acute interstitial nephritis triad
- fever, rash, eosinophilia (rare)
arthralgia - mild renal impairment
- hypertension
Labs/urine: Acute interstitial nephritis
WBC, WCB clasts
Labs/urine in ATN
Muddy brown clasts
Epithelial cells
Outcomes of CKD
Electrolytes
Lipids and RBC
- Lose H+, K+,
–High serum phosphate (as not excreted) = low Ca lead to high PTH
retain Na and H20 (= oedema, HTN, HF peri& lung oedema),
Uremia (asterixis, encephalopathy )
* Increase in Lipids
* Reduced production of EPO = Bone marrow not stim to produce RBC = normocytic normochromic anemia additionally they have an iron deficiency note rx EPO = increased bl. Pressure
Hyperacute rejection (minutes to hours)
- Which anti-‘s involved
-type of hypersensitivity rnx
- Results
Hyperacute rejection (minutes to hours)
- pre-existing antibodies against ABO or HLA antigens
-Type II hypersensitivity
=widespread thrombosis of graft vessels → ischaemia and necrosis of the transplanted organ
Rx: graft must be removed
Acute graft failure (< 6 months)
Cause
SX/Lab
- mismatched HLA. Cell-mediated (cytotoxic T cells)
usually asymptomatic ;rising creatinine, pyuria & proteinuria - cytomegalovirus infection
may be reversible with steroids and immunosuppressants
Causes of chronic graft failure (> 6 months)
both antibody & cell-mediated = fibrosis to the transplanted kidney (chronic allograft nephropathy)
recurrence of original renal disease (MCGN > IgA > FSGS)
Relative importance of HLA antigens in transplant
HLA antigens are as follows DR > B > A
Renal transplants CMV infection
20%
6-12wk after transplant
Renal transplants CMV infection prophylaxis & rx mild infections
valganciclovir
Sx of severe CMV infection & Rx
myocarditis, encephalitis, retinitis
ganciclovir
Prophylaxis of PJP in renal transplant
co-trimoxazole for 6 mo
Drug that alter the blood flow to the Kidney
NSAID Prostaglandins reduce bl to kidney
ACEi & ARB-
Ciclosporin & Tacrolimus
Drugs that have tubular toxicity (ATN)
Aminoglycosides
Cisplatin
Amphotericin
What does lithium desensitizes the kidney’s ability to
respond to ADH in the collecting ducts
DI (h20 = low, dex= low )
ADPKD type 1 gene
chromosome 16 = 85% of cases
ADPKD type 2 gene
Chromosome 4, later renal failure
Screen in family and Rx of ADPKD
screening investigation for relatives is abdominal ultrasound
tolvaptan (vasopressin receptor 2 antagonist)
What is a normal anion gap
(sodium + potassium) - (bicarbonate + chloride)
A normal anion gap is 8-14 mmol/L
management of proteinuria in CKD
ACEi & SGLT-2 inhibitors
Anti-phospholipase A2 antibodies are associated with
Idiopathic membranous glomerulonephritis
renal biopsy demonstrates a thickened basement membrane with subepithelial electron dense deposits on electron microscopy.
membranous glomerulonephritis
Membranous glomerulonephritis Causes (5)
- idiopathic: due to anti-phospholipase A2 antibodies
- infections: hepatitis B, malaria, syphilis
- malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
- Drugs: gold, penicillamine, NSAIDs
- Autoimmune diseases: SLE (class V disease), thyroiditis, RA
Extra-renal manifestations of ADPKD
Liver cysts
berry aneurysms (8%)
Mitral valve prolapse
Reduces renal perfusion in HF causes
High levels of aldosterone
what causes Causes ‘swimmer’s itch’
Sx
risk factor
Rx
Schistosoma haematobium
From snails, flukes
- frequency, haematuria. Risk factor for squamous cell bladder cancer
Praziquantel
What causes Renal cell cancer
- more common in middle-aged men
- smoking + obesity
- Mutations chrom 3
- von Hippel-Lindau syndrome
- tuberous sclerosis
Where does Renal cell cancer start
proximal convoluted tubule’s epithelial cells
most common type of RCC ?
is a clear cell carcinoma
How does RCC led to a left varicocele?
& Why cant it happen on the right
RCC invades the left renal vein, then the venous drainage of the left testis is blocked, leading to a varicocele.
his can never happen on the right side, because the venous drainage from the right testis goes directly into the inferior vena cava.
RCC associated paraneoplastic syndromes
- Erythropoietin=polycythaemia,
- PThr =hypercalcaemia,
- Renin= HTN,
- ACTH= cushing syndrome
Stauffer syndrome.-paraneoplastic hepatic dysfunction syndrome. Typically presents as cholestasis/hepatosplenomegaly. It is thought to be secondary to increased levels of IL-6
Rx RCC
- surgery or ablation of the tumor can be done.
If there’s metastasis, then immunotherapy with aldesleukin or targeted therapy can be done in selected cases.
Calcium phosphate
- Ass
- Imaging
-Urinary acid
- Rx
Assoc w/ RTA 1&3,
Urinary acid: Normal- alkaline
Radio-opaque stones (composition similar to bone)
RX : low Na diet & Thiazides
Calcium Oxalate stone
- Ass
- Imaging
-Urinary acid
- Rx
Most common cause of stones
Risk factors: Hypercalciuria, Hyperoxaluria, Hypocitraturia (citrate forms complexes with ca2+ making it more soluble)
- radio-opaque
- associated w/ short bowel syndrome, antifreeze, vitamin C abuse
Urinary acid : Variable
Rx: Thiazide diuretics Potassium citrate, low Na diet
* cholestyramine reduces urinary oxalate secretion
* pyridoxine reduces urinary oxalate secretion
Urate stones
- Ass
- Imaging
-Urinary acid
- Rx
Caused: d’s w/ extensive tissue breakdown/turnover e.g. malignancy, gout, Dehydration, leukaemia, children with inborn errors of metabolism
Urinary acid: Acid
Radiolucent (No seen)
Rx: Alkalinization (bicarb) of urine, allopurinol
Struvite stone/ Magnesium ammonium phosphate
- Ass
- Imaging
-Urinary acid - Rx
Presents as infection formed by urea-splitting bacteria,
-Proteus,
-Staph saprophyticus,
- klebsiella
Often staghorn calculi =chronic obstruction and failure to clear UTI adequately
Urinary acid : Alkaline
Radiopaque
Cystin Stones
- Ass
- Imaging
-Urinary acid
- Rx
in patients with inherited cystinuria
Moderately radiopaque
Urinary acid : Normal
Rx of renal stones
Stones < 5 mm will usually pass spontaneously.
Lithotripsy and nephrolithotomy may be for severe cases.
When are stones an emergency
Rx (3)
Ureteric obstruction + infection =surgical emergency
-nephrostomy tube placement,
-insertion of ureteric catheters
- ureteric stent placement)
Wilms tumor/nephroblastoma
Mutation
- early childhood and appears between the ages of 2 to 4.
- The tumor contains embryonic glomerular structures
- mutations of tumor suppressor genes WT1 and WT2 on chrom 11
Causes of painless Hematuria
Transitional Carcinoma of the Bladder
Squamous Carcinoma of the bladder
Causes of squamous cell carcinoma of the bladder (4)
Scsc
Causes of transitional cell carcinoma of the bladder (4)
Causes of transitional cell carcinoma of the bladder (4)
Rx Minimal change disease
oral corticosteroids: majority of cases (80%) respond
cyclophosphamide is the next step for steroid-resistant cases
Renal transplant which HLA matching is most important
DR
Diffuse proliferative glomerulonephritis, causes (2)
post-streptococcal
SLE
Indication for renal replacement
