Tubular Anatomy Flashcards by kavin Athithya

What are all the renal compartments?

Tubules and interstitium—— 85%

Glomerular compartment——10%

Vascular compartment——-5%

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What does renal corpuscle consist of?

Glomerulus + Bowman’s capsule

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What does Proximal tubule consist of ?

1) Proximal convoluted tubule (Pars convoluta)

2) Proximal straight tubule (Pars recta)

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What does intermediate tubule consist of ?

1) Thin descending limb of loop of Henle

2) Thin ascending limb of loop of Henie

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What does Distal tubule consist of ?

1) Thick ascending limb of loop of Henlie (Distal straight tubule)

2) Distal convoluted tubule

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Excretory part of kidney consist of

Proximal tubule

Intermediate tubule

Distal tubule

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Collecting part of kidney consist of

Connecting tubule

Cortical collecting duct

Outer medullary collecting duct

Inner medullary collecting duct

Ureter

Pelvis

Calyx

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What are the type of nephrons?

Cortical nephrons ( Short looped) 85%

Juxta medullary nephrons (long looped) 15%——Major role in urine concentration

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Maximum reabsorption of “all” ions occur PCT only true or false

False, majority of Mg absorption occur in thick ascending limb of loop of Henlie.

Majority of all other ions absorption occur in PCT only

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What are important transporters in PCT ?

1) Passive Paracellular transport h20 na mg ca k

2) Secondary active transport (Antiports)

Na dependent Amino acid transport
Na dependent glucose transporter sglt 2
Na dependent phosphate transporter type 2

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Why PCT damge may cause renal rickets?

Phosphorous is handled only in PCT so if there is PCT damage then phosphorous cannot be absorbed so there is rickets manifestations

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H20 + CO2———- H2CO3 Enzyme used for this reaction

Carbonic anhydrase type 2

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H2CO3——–H2O +CO2 Enzyme used for this reaction

Carbonic anhydrase type 4

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Global dysfunction of PCT called

Fanconi syndrome/ Renal Tubular Acidosis type 2 / proximal RTA

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Fanconi syndrome type of inheritance

Autosomal recessive

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How will you describe fanconi syndrome age wise appearance ?

In children M/C Cystinosis

In Adolescents M/C Wilson’s disease

In adults M/C Drug induced

In elderly M/C Multiple myeloma

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Inherited causes of fanconi syndrome

Cystinosis
Wilson’s
Galactosemia

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Drugs causing Proximal RTA

Ifosfamide
Cisplatin
Tenofovir
Valproate

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Drugs causing acidosis without causing PCT dysfunction

Topiramate

Actazolamide

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Clinical manifestations of Proximal RTA

1) Renal rickets due to phosphorous loss

2) Euglycemic Glycosuria (PCT is not working so reabsorption is impaired)

3) wasting and growth retardation due to amino acid loss

4) Normal anion gap metabolic acidosis (due to HCO3 loss in urine)

5) Salt and Water depletion causes severe dehydration and secondary raas activation and aldosterone increase which results in hypokalemia

6) Risk of CKD is minimal because of minimal proteinuria

7) Hypouricemia

8) Hypocarnitinemia

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What is anion gap and how it is affected in Proximal RTA

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Anion gap = Na - (Cl +HCO3)

In Proximal RTA bicarbonate is lost due to non absorption in PCT, to compensate the bicarbonate loss Cl is increased, so hyperchloremic acidosis occur

Comment about urine ph in Proximal RTA

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Acidification of urine is normal, because the acidification is mainly done by intercalated cells

So ph of urine in Proximal RTA is 4-4.5

Why no significant acidosis occur in proximal rta ?

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Some of the Bicarbonate ions are reabsorbed in distal segments so no significant acidosis occur in proximal rta

Types of cells in cortical collecting duct

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1) P-cell (Principal cell)
2) alpha-intercalated cells
3) Beta- intercalated cells
4) un-named cells

Transport mechanisms in P - Cells

1) enac channels These are aldosterone induced epithelium na channels 2) romk somk these are uniports which governs movement of k and H from p cells to luminal side

Enac channels MOA

Aldosterone released from zona glomerulosa----- they go and act on intra cellular aldosterone receptors ------- production of AIPs (Aldosterone Induced Proteins)------- they activate Enac channel which governs movement of na and h20 inside p cells and k or h+ to luminal side

Excess aldosterone produces what syndrome

Conn's syndrome

Conn's syndrome triad

HTN Hypokalemia Metabolic alkalosis

What does hypo aldosteronism cause ?

RTA type 4

How can you suspect RTA type 4 / hypo aldosteronism

1) Hyperkalemia without renal failure 2) Hyperkalemia disproportionate to degree and duration of renal failure------ in simple words massive Hyperkalemia even in small renal failure

What are the two main types of hypoaldosteronism?

True hypoaldosteronism and Pseudohypoaldosteronism (PHA)

What are the subtypes of true hypoaldosteronism?

1) Hyporeninemic hypoaldosteronism (↓Renin ↓Aldo) 2) Hyper-reninemic hypoaldosteronism (↑Renin ↓Aldo)

Causes of hyporeninemic hypoaldosteronism?

1. NSAIDs 2. β-blockers 3. Aliskiren (Direct Renin inhibitor) 4. Diabetes mellitus A) Autonomic neuropathy ( β receptor dysfunction) B) Prorenin not converted to renin)

Causes of hyper-reninemic hypoaldosteronism?

1. Adrenal insufficiency (Addison's disease) 3. Drugs: ACE inhibitors, ARBs,Aldosterone synthase inhibitors (Heparin, Ketoconazole)

What are the types of Pseudohypoaldosteronism (PHA)?

Acquired PHA Inherited PHA (Type 1 and Type 2)

Causes of acquired Pseudohypoaldosteronism?

1) Chronic tubular interstitial fibrosis (they may cause fibrosis of beta receptors) -Vesico-ureteral reflux, -Obstructive nephropathy, 2) Drugs producing fibrosis (Calcineurin inhibitors) 3) Aldosterone receptor blocker Spironolactone, Eplerenone 4) Enac Channel blocker Amiloride, Triamterene, 5) Trimethoprim (Similar Structure to triamterene) 6) Pentamidine

Which drug is a direct renin inhibitor?

Aliskiren

What are types of inherited PHA

Type 1 Type 2

What are renin stimulators?

Prostaglandins, β-receptors, Renal hypoperfusion

Which enzymes and transporters are involved in α-cell function?

Carbonic anhydrase II H+-K+ ATPase H+ ATPase

Which transporters are involved in β-cell function?

Pendrin channel Anion exchanger

What are the main inherited defects in Type-1/Distal RTA?

Autosomal fominanay Anion exchanger defect, Autosomal recessive H+ ATPase defect/H+K+ATPase defect

What is a common syndrome associated with acquired distal RTA?

Sjögren’s syndrome

Which drug causes acquired distal RTA?

Amphotericin B Toluene

What are the clinical features of distal RTA?

1) Most common in children 2) RFT normal 3) inability to acidify urine, 4) NAGMA

What is a key lab finding in distal RTA regarding urine pH?

Urine pH > 5.5 for 3 consecutive days

What bone-related complications occur in Type-1 RTA?

Osteopenia, bone deformities, rickets

What is the reason for hypokalemia in distal RTA?

Salt and water wasting leads to decreased renal perfusion → secondary hyperaldosteronism → hypokalemia

What causes stone formation in distal RTA?

Hypercalciuria, hypocitraturia, medullary nephrocalcinosis

What is the significance of hypocitraturia in distal RTA?

It contributes to calcium stone formation

Which enzyme defect is seen in Type-4 RTA?

Carbonic anhydrase II

What are some features of Type-4 RTA?

Osteopetrosis, dense bones, mental retardation, cerebral calcification

Tubular Anatomy Flashcards

(52 cards)