Renal Flashcards by Rachel Longwell

What are the general features of a RTA

Why are they short

What is the general mainstay of treatment

Metabolic acidosis
Normal anion gap
High serum chloride

Boney phosphate is being used as a buffer

Replace bicarb
Furosemide for type 4

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Where is the defect in a type 1 RTA
what will you see in the serum and urine
What is the classical age of presentation and how?
What can cause it

Distal convoluted tubule-impaired h+ secretion

Metabolic acidosis, urine is alkalotic, hypokalaemia, high urine calcium, high serum chloride

Stones, polyuria, rickets and FTT. 1st year of life

Medullary sponge kidney

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Where is the defect in type 2 RTA?

What is seen in the serum and urine?

What is the syndrome associated called?
What are the congenital and acquired causes?

What is Lowe syndrome otherwise known as?

How does cystinosis present

Proximal convoluted tubule

Metabolic acidosis, high serum chloride, acidic urine, no stones, glucose, protein and amino acids in urine. Low serum K

Fanconi syndrome
Metabolic disease, cystinosis, heavy metal poisoning, chemo agents, gent, ranitidine, amyloid, myeloma

Occulocerebral renal syndrome
X linked recessive
Cataracts, behaviour change, growth failure

Photophobia and retinal detachment, hypothyroid, rickets

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Where is the defect in type 4 RTA?

What is seen in blood and urine

Blocks aldosterone

Metabolic acidosis with acidosis urine hyperkalaemia, High urine sodium

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What are general rules of thumb for transporter defects?

Metabolic alkalosis

Hypokalaemia

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What diuretics do barters and gitlemans act like

What is another name for Lidle syndrome

Barters- like loop
Gitlemans- like thiazides
Liddle- pseudohyperaldosteronism

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Where is the defect in barraters syndrome? What gets activated making things worse

When and how does it normally present?

What is seen in blood and urine

What might you see on renal biopsy?

Which subtype has deafness?

Which diuretic does it mimic? How do you know it’s not diuretic abuse?
How is it treated

Ascending Limb of henle Na-k-cl transporter RAAS

Birth- polyhydramnios, poor growth, polyuria and ? Stones

Infantile- polyuria,ftt

Metabolic alkalosis, high urine calcium, chloride, sodium and potassium
hypokalaemia and low serum chloride

Hyperplasia of the JGA

Type 4

Loop- BP normal
Replace electrolytes and give k sparing diuretics. NSAIDs to reduce prostaglandin

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How is baratters syndrome treated (2 things)

Give sodium and potassium supps

Give NSAIDS- switches off the prostaglandin effect

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Where is the defect in Gitleman syndrome?

What is seen in blood and urine

When does it present?

What diuretic does it mimic?

What might it overlap with?

DCT

Metabolic alkalosis, low serum magnesium, low urine ca

Adolescence

Thiazides

Type 3 barrters

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Liddle syndrome
Where is the defect
What is seen on bloods
What measure is important in diagnosis

Collecting duct
Hypokalaemia, metabolic alkalosis and low RAAS
HYPERTENSION

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What is the normal daily requirement for sodium

3mM/kg/day

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How do you calculate osmolality

What is normal-

2xna + urea + glucose

280-320

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How fast should hypernatraemia be corrected

No faster than 0.5mmol/ hour

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How do you distinguish between renal and non renal causes of hypernatraemia
What is the calculation
What is normal

Urinary fractional excretion of sodium
High- renal issue- DI or HONK
Low not renal issue- diarrhoea or fever

Urine sodium x serum creat/ urine create serum Na
1%

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What are the features of DI on blood and urine?

What causes DI

Hyperna , high serum osmolality, low urine osmolality

Not enough ADH- water can’t be reabsorbed

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In DI what should be seen on a water deprivation test

When should the test be stopped?

Low urine osmolality (<700)
High serum osmolality (>300)
>3% weight loss

Too much weight loss

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What is DDAVP?

What should it show?

Synthetic adh
No effect if nephrogenic
If central should increase urine osmolality by 50% or more

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What are central causes of DI

Brain tumours or post pit dysfunction

Structural- SOD

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What is the most likely genetic cause of nephrogenic DI

How is it treated

X linked- mutated adh receptor

Drink Lots of water, low sodium diet, diuretics

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Why is desmopressin given in nocturnal enuresis

Brain hasn’t learned to turn on ADH overnight causing nocturnal enuresis

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How do you calculate an anion gap?
What is normal?
What does a normal gap indicate?
What does a high gap indicate?

Na+K - Cl+HCO3
10-12
Loss of bicarb
Addition of h

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How is DI treated

Low sodium diet, thiazides diuretics, NSAIDs

Desmopressin if central cause

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What are causes of a high anion gap

Methanol
Uraemia
Dka
Paraldehyde 
Isoniazid 
Lactic acidosis 
Ethylene glycol 
Salicytes

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What are causes of a normal anion gap

What are the two most common causes

Addisons
Bicarb loss
Chloride Xs
Diuretics

GI losses or RTA

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Excess of which 2 diuretics will cause a metabolic alkalosis Which 2 will cause a metabolic acidosis

Furosemide and thiazides Acetazolamide and k sparing

What do you see in the blood with laxative abuse. | How is this different from normal diarrhoea

Hypokalaemia and metabolic alkalosis Usually also increased Mg Normally diarrhoea causes a normal anion gap metabolic acidosis

Define elevated blood pressure What is stage one What is stage 2

Blood pressure greater than the 90th centile >95th centile >95th plus 12

What is the best pharmaceutical treatment for htn in children What is the best treatment for hypertensive urgency. What classes of drugs are they “Urgency

``` Ace inhibitor Oral isradipine (calcium channel blocker) Iv hydralazine (vasodilator) Iv labetalol (beta blocker) or sodium nitroprusside ( vasodilator) ```

What percentage of PUVs go on to ESRF What percentage have VUR How are they managed

30% 50% Relief of obstruction and monitoring renal function. Laser ablation

Where does UPJ obstruction normally occur | What normally causes it

L sided | Intrinsic compression from an artery

Outline the RAAS system | What is the role of ANP

Renin secreted from JG cells when the macula densa at DCT senses low Na or the efferent arteriole senses low Bp Stimulates AT1 release from the liver. ACE from lungs causes conversion to AT2- causes vasoconstriction Stimulates- aldosterone- CD- increased Na in exchange for K. ADH- increases aquoporins in CD to increase water reabsorb ANP- released when fluid overloaded- reduces Na so less renin-more naturesis

Which syndrome is a horseshoe kidney associated with | What tumour is it associated with

Turners | Wilms-4x increased risk

``` AR cystic kidney disease How does it present What is seen on ultrasound What other organ is affected When does end stage renal disease usually start ```

Bilateral flank masses. Feeding difficulties or breathing issues if severe Lack of corticomedullary differentiation and bulky kidneys Liver- fibrosis 12 years

AD PKD | What other organ may have cysts

Brain- Berry aneurysms causing SAH

What is nephronoptosis What is the usual phenotype What happens the kidney over time What is the gene associated

Medullary kidney cysts Red hair,FTT and fanconi syndrome Gets smaller causing CKD NPHP1

What three kidney things are seen with TS

Simple cysts Angiomyplipomas Renal cell carcinoma

Outline the 3 stages of AKI

1- creat 2x baseline 2-2-3x baseline, u.o less than half ml/kg over 6-12h 3-3x plus with anuria

What are the features to look for in AIN

Sterile pyuria, global tubular dysfunction and uveitis

What fluid should be replaced in aki | How is insensible loss calculated

Insensible loses with urine output and all other loses | 400ml/m2/day

What is the most likely bug in PD peritonitis | What is the first line abx regime

Strep pneumonia and E. coli | Cefazolin and ceftazidime

What are the 2 main side effects of cyclosporine

Hirsuitism | Gingival hypertrophy

What are the 2 main side effects of tacrolimus

Alopecia Diabetes Low Mg

What are three main side effects of MMF

Lukopenia, anaemia, GI side effects

What is characteristic about haematuria in alports disease Genetically what occurs What are other phenotypically features

Microscopic, becomes macroscopic with infections X linked, type 4 collagen defect SN hearing loss and anterior lenticonus

What happens in thin basement membrane disease | Will it progress to ESRF

Persistent microscopic haematuria | No!

What is the classical presentation of HSP What is it What is a sign of poor prognosis How long should urine dip and BP be monitored for What might be useful to treat it

``` Swelling and haematuria 1-3 weeks after URTI IgA mediated small vessel vasculitis Nephrotic range protein at diagnosis 12 months Steroids ```

When after a strep infection is PSGN usually seen What happens complement levels What would be seen on biopsy

10d after throat infection, 3 weeks after cellulitis Low Neutrophil infiltration

How is igA nephropathy differentiated from post infectious (2 ways)

Haematuria at the time of the infection | Normal complement levels

What are three causes of low complement in GN

PSGN Mesangiocapillary SLE

What is cresentic GN also known as

Rapidly progressive

In good pastures what are antibodies formed against

Type 4 collagen in basement membrane

What is the triad of HUS | What happens to haptoglobins

AKI low platelets and microangiopathic haemolytic anaemia | Low!

What infection can cause atypical HUS | What neutrophil count shows poor prognosis

Pneumococcus | Neuts >20

What complement pathway is involved in complement mediated HUS WHich MAB is useful

Alternative pathway | Ecilizumab

What is AIN what are the characteristic features What is TINU What drugs can cause it

Immune mediated kidney infiltration with inflammatory cells. Causes tubular damage General tubular dysfunction, sterile pyuria, tired with polyuria With uveitis NSAIDs, PPIs, antibiotics and diuretics

Loop diuretics Give an example Where do they work How do they work What is seen in the blood with excess What diuretic works in a similar way with similar side effects Where do they work

Loop of henle and DCT Block nakcl transporter- keep na and k in the lumen and water follows Hypo k and na Metabolic alkalosis High urine mg and ca Thiazides-DCT

K sparing diuretics How do they work What 2 main things are seen in blood

Block aldosterone | Hyper jalapeños and metabolic acidosis

Nephrotic syndrome Why is there an associated immunodeficiency? What infections are most common

Reduced production of immunoglobulins | Encapsulated

Nephrotic syndrome | Why is there an associated hupercoagulability and high cholesterol

Reduced oncotic pressure therefore reduced liver perfusion Raised VLDL raised clotting factor production

Nephrotic syndrome What dose of steroids is given and for how long What defines a relapse What defines remission What defines steroid dependence What defines steroid resistance- what is the risk to developing CKD

60mg/m2 for 6 weeks >3+ protein over 3 consecutive days Zero or trace protein “ Relapse on steroids or less than 2 weeks off No improvement after 4 weeks- around 40 %

What stain is likely to pick up FSGS

Trichrome staining

Which three renal diseases can recurr in transplant | Which can change to another

FSGS, membranoproliferative, and 1/3 of igA Alports- becomes anti GBM disease

Congenital nephrotic syndrome What is the most common genetic cause What is another cause

NPHS1 | WT1

Which type of stones are most common What happens citrate and Oxalate in the urine What can cause them- 4 things and 2 meds

Calcium stones- oxalate and phosphate High oxalate, low citrate Malabsorption and short gut, RTA, hyper PTH TOPIRAMATE AND ACETAZOLAMIDE

What causes cysteine stones Which 4 amino acids leak Into the urine What causes Uric acid stones What causes struvite stones What type of stone is likely to cause a staghorn calculus

Cysteinuria- cystine, ornithine, arginine and lysine Lesch nyhan syndrome UTIs Struvite stones

What is dent disease What are three main features Which 2 genes are affected

X linked form of fanconi syndrome Haematuria, polyuria and stones OCRL1 CLCN5

What medication is useful for giggle incontinence

Oxybutinin

What does the mesonephros form | “ metanephros

``` Ureteric bud (pelvis and collecting ducts) Everything else ```

What does DMSA show | What do mag 3 and DTPA show

Structure and scarring | Function (?obstruction)

What type of drugs are cyclosporine and tacrolimus

Calcineurin inhibitors