Why is urine pH low (<5.4) in RTA II? I thought pH would be ↑ since HCO3- cannot be reabsorbed and will remain within the tubule.
Thanks a lot in advance.
This is due to aldosterone resistance or deficiency. Thus, Enac is inhibited, which decreases negative charge, which results in less H+ being excreted into the lumen.
If there is less H+ being excreted, how is the pH of the urine < 5.5?
Im just bitching because ive been buying citrate pills off amazon and i cant afford them because my SSI got discontinued.... My bones hurts and i cant sleep...
I had repeated kidney stones after taking lithium (for bipolar/depression) , and i have PFD and vulvodynia as complications of being on antibiotics for utis (because they wouldn't let me see a damn urologist and nobody believed me... I brought in the stones and they shoved me to another doctor)
I finally got into see a urologist... But i am more than nervous. My ssi got discontinued in may (i was on it original for depression/anxiety and havent been able to get to doctors appointments because of pain LOL) and it has stressed me to the brink..like. I want to work. But the pain keeps me up some night. I still struggle with depression anxiety and my pt actually said my anxiety is probably causing my pelvic floor dysfunction.
Im frustrated because its not like im trying to be some lazy person. I took prazosin and was bedridden all morning. I restricted my eating and my bones are popping every.move i make. I bought pottassium and magnesium citrate and to be HONEST it just fucked with my stomach and now i have kidney pain.
Texas also banned delta 8 and it was the only legal thing that made a difference.
Im so tired and angry and sick. I would go inpatient for depression but doctors wont manage my pain anyways.
My therapist lowkey told me to buy weed if it helped.
Im on a concoction of things that more or less work but life happens (like my multivitamin citrate out of stock) or one of my closest friends (even if we werent in contact) dying last week and being unable to keep up. Or my grandparents emotionally abusing me and making me terrified to leave the house.
SSI lying to me that my disability was pending so i didnt file an appeal, the urologist secretary telling me they suddenly decided to not take medicaid, or that my gp didnt send a refferal, getting 6 months to get a pt appointments bc they only schedule every 3 weeks and i had ring worm/vulvodynia/and an asthma attack consecutively at every appointment.
I went to the er about 8 times and they screened me for a uti and told me to go home and see a specialist. Ive had anal fissures and GI problems and other gross things but people act like its taboo and gross and strange.
I feel like im getting fucked on every end and im genuinely not sure how im expected to not be depresses.
I read that inactivating mutations in the gene encoding carbonic anhydrase 2 cause a combination of proximal (type 2) and distal (type 1) renal tubular acidosis (type 3 RTA). So, I was wondering why carbonic anhydrase inhibitors (eg. acetazolamide) are only associated with proximal (type 2) RTA instead of proximal+distal (type 3) RTA.
Thanks in advance.
This vignette has been modified.
A 50 yo patient has 3 days of decreased urination, headache, and nausea.
Labs are:
- Na+ is 137
- K+ is 3.2
- Cl- is 116
- Urine pH 7.0
ABGs are pH of 7.28 and HCO3- of 14. This patient likely has has prolonged treatment with which drug?
A. TMP-SMXB. acetazolamideC. eplerenoneD. amphotericinE. heparinCorrect answer is D. amphotericin
Apparently, this pt has Type I RTA, which somehow ties to why choice D. is correct.
My Q's
- I know the pt has normal A-G metabolic acidosis and hypokalemia (eliminate choice C). But, the vignette itself offers basically no context clues. ...how are you supposed to know when to start thinking about RTA?
- According to the explanation, some choices are incorrect b/c they correspond to a different RTA than the one this patient has. But again, I'm confused.. How are you supposed to know when to start thinking about RTA? ...like, I didn't even have RTA on my radar, so I didn't know to eliminate choice B b/c CAI's = type II RTA and choice E b/c heparin = type IV RTA, etc.
Any good video lecture or material
If there is lack of aldesterone ( and therefore lack of excreting H+ ) And lack of excriting NH4+ ( which is a way to secrete acid ... if i am not wrong here maybe this is where i am mistaken , it puzzles me )
Then how does the urine become acidic ph < 5.5 ?
Bit of a long shot but i was hoping a pun might throw more people my direction
just reading up on renal tubular acidosis and i couldn't find out why its described as a hyperchloraemic acidosis.
does anybody have a mechanism for the high chloride levels?
Why is there acid urine in RTA type 2 if there is reduced resorption of HCO3? Shouldn't it be alkaline? Also how is hypercalciuria manifested in type 1?
Specifically:
"Spilled alkaline substance on inside track: CA inhibitors (acetazolamide) cause bicarb to stay in the tubular lumen leading to urine alkalization"
"Two tubes of acid: CA inhibitors cause a type 2 renal tubular acidosis (defect in proximal bicarb reabsorption)"
Who has the best explanations of the various renal tubular acidosis and why the pH, K+ levels, etc are high/low?
I can memorize this stuff, but I imagine knowing the why will not only let me remember it better but also make those up down arrow questions much easier. Thanks.
So I've had repeated UTIs since March and chronic kidney pain and muscle weakness since November. Sometimes the pain flares horribly. Should I get checked for RTA?
Why the hell is there hypokalemia if h+ secretion is inhibited in rta type one.
