And So It Begins 

I was looking for some notes I’d made for today’s blog and couldn’t find them. Okay, so my office is being rearranged. After a few minutes of my kind of cursing [quite inventive, if I do say so myself], I accepted that I would just have to recreate them. Certainly not from memory since chemo brain and chronic kidney disease brain fog share the space in my brain. Yep, I was going to go back to the internet and research the topic all over again. 

But I didn’t. I stumbled upon some information that blew me away. I had never wondered about this, not even a little. What is it, you ask. Let me answer your question with a question: Have you ever wondered how your kidneys came to be? That’s the information I stumbled upon, and it fascinated me. We’ll probably have to rely on quite a few definitions, but it’s still worth exploring. I’ll place the definitions in brackets next to the word being defined. They were gathered from my own brain and various sources. 

Duke Medical’s site is what sparked my interest: 

“Ascent of the kidneys 

The kidneys initially form near the tail of the embryo. 

Vascular buds from the kidneys grow toward and invade the common iliac arteries [the ones that carry blood to the lower extremities]. 

Growth of the embryo in length causes the kidneys to ‘ascend’ to their final position in the lumbar [the lower spine and the part of the back near it] region. 

Rather than ‘drag’ their blood supply with them as they ascend, the kidneys send out new and slightly more cranial [Of or relating to the skull or cranium] branches and then induce the regression of the more caudal [a. Of, at, or near the tail or hind parts; posterior: the caudal fin of a fish. b. Situated beneath or on the underside; inferior.] branches.  

This is a highly regimented procedure. What if something goes awry? What could happen then? Back to Duke Medical for some possible answers:  

“A. Duplication of the urinary tract 

Occurs when the ureteric bud [what eventually becomes the ureter] prematurely divides before penetrating the metanephric blastema [the other part of the embryo that becomes part of the kidney, usually the nephrons]. 

Results in either a double kidney and/or a duplicated ureter and renal pelvis [“The renal pelvis is a chamber where all the urine-forming ducts meet and further routes urine to the urinary bladder.” Mansi Kohli.] 

B. Renal-Coloboma syndrome 

The Pax2 gene essential for metanephric mesenchyme [later to become nephrons, the filters in your mature kidneys] to differentiate into epithelial tubules [“Renal tubular epithelial cells are resident cells in the tubulointerstitium [connecting tissue between the cells in the tubules] that have been shown to play crucial roles in various acute and chronic kidney diseases.” National Library of Medicine.]  in response to inductive signals from ureteric bud, so mutations (even if HETEROZYGOUS [Two variations of a gene on the same locus of a chromosome]) can produce renal defects.  Patients typically exhibit the following symptoms: 

Renal hypoplasia [incomplete development] – due to reduced proliferation of the mesenchyme [tissue found in organisms while they develop] derived epithelia [body tissue that covers all surfaces of your body, inside and out] during development. 

Vesicouretral Reflux [Urine flows backwards up into the kidneys and ureters from the bladder] – most likely due to improper connection of the ureter to the bladder or possibly due to inherent defects in epithelial cells of the mature ureter.              

Colobomas (ventral fissures in iris, retina, and/or optic nerve) – due to failure of the optic fissure to fuse (expression of Pax2 is observed in ventral part of the optic cup and optic stalk). 

C. Nephroblastoma (Wilms Tumor) 

found in infants from 0-24 months of age 

consists of blastemal [a mass of cells that is capable of becoming an organ or appendage], epithelial, and stromal [supporting tissue] cell types 

associated with mutations in genes related to kidney development (PAX2, WT1, etc.) 

essentially due to incomplete mesenchymal-to-epithelial transformation (i.e. the cells fail to fully differentiate and transform into cancerous cells). 

D. Polycystic kidney disease 

can arise due to a variety of factors: 

loss of polarity: aberrant differentiation of tubule cells results in inappropriate location of Na/K [sodium/potassium] channels to the apical [apex] (rather than basal [base]) domain of the cells.  Na+ is pumped apically, water follows resulting in dilation of tubule lumens [part of the nephrons, have no red blood cells]. 

Overproliferation: excessive growth of tubule epithelium can occlude the lumen causing blockage.” 

You have been incredible today reading a blog with all the definitions stuck in the descriptions. Thank you for bearing with me on that. I feel the mystery has been solved. I hope you do, too. Knowing how kidneys are formed, believe it or not, makes me feel more appreciative of them – even though I was already very appreciative of them. 

With the holidays coming up, I’m going to be that nag who reminds you to take care of your kidneys. Watch your renal diet. Get adequate sleep. Try not to smoke or drink. Exercise even though you don’t want to. And most importantly of all, don’t let the stress get you. Avoid it, minimize it, do whatever you can to stay … without smoking or drinking. 

The next blog will be on the 19^th, which means it will be during Chanukah. Christmas and Kwanzaa won’t be far behind. Have I left out whatever holiday you observe? Let me know. Hmm, maybe next week’s blog should be about holiday meals. 

Until next week, 

Keep living your life!