Interstitial cystitis (IC) Surgery

General Information

Surgery is generally considered the treatment of last resort by IC patients and their doctors. The obvious reasons are that surgery is invasive and irreversible, but in addition, many patients who choose to have surgery may not improve, and some may, in fact, do worse. Potential complications from these procedures also need to be considered. Researchers have pointed out that with an ever-enlarging array of treatment options available to the IC patient, surgery should be considered only when all other choices have failed. This Fact Sheet is intended to be a brief overview of the most common methods available. Only a urologist experienced in treating IC can advise you as to the appropriateness of surgery for your particular situation.
 

Types of Surgery

    There are two basic types of surgery used in IC patients: augmentation cystoplasty and urinary diversion.
    In augmentation cystoplasty, part or most of the bladder is surgically removed and replaced with a section of the patient's bowel, thus forming a "new bladder." Urine continues to be stored in the bladder and evacuated through the urethra.
    Urinary diversion is performed in several ways: With the bladder either removed or left in place, a tube or conduit is fashioned from a short section of bowel and the ureters are placed in this conduit. The urine is then diverted to an opening in the abdomen called a stoma, through which urine is allowed to drain constantly into a collection bag.
    In a second type of procedure, also with the bladder either removed or left in place, an internal pouch (known as a Koch, Florida, or Indiana pouch) is constructed from a bowel segment and placed inside the abdomen. The urine is emptied from the pouch by self-catheterization four to six times each day.
 

Clincal Studies

Little data is available on the long-term outcome of these surgical procedures. A small study done at Duke University  reviewed the cases of IC surgery patients. Many augmentation patients continued to have urgency and frequency, and some were unable to void on their own, necessitating self-catheterization, which was often difficult. IC has also been reported to recur in the augmented bowel segment of bladders. Some patients who undergo total cystectomies (bladder removal) still experience pelvic pain, indicating that neurologic mechanisms are an important aspect of IC that needs to be researched further.
 

Who Can Benefit

    Most of the current available literature concludes that surgery should be reserved as the treatment of last resort, and used primarily in patients for whom decreased bladder capacity (less than 250cc under general anesthesia) is the primary problem.
    Patients who have only bladder pain related to filling seem to benefit more than those who have more generalized pelvic, urethral, vaginal or labial pain and those with larger capacities.
 

Some Questions to Ask Your Doctor

•     What are the known complications of the procedure?
•     What is the specific condition of my bladder: capacity, presence of ulcers, fibrosis?
•     Are there other treatments I should try, including pain management techniques, before I consider surgery?
•     Should I have psychological counseling before I decide on surgery? How do I prepare myself for surgery?
•     What are the chances I will still have IC pain after this surgery? If I continue to have pain, how can it be treated?
•     How will my bowel function be affected by this surgery? Will my kidneys be affected after the surgery?
•     Who long will the surgery take, how long will my hospital stay be, and how long is the recovery period?
•     How will my activities be restricted after surgery?
•     What conditions require further surgery and what are the chances I will need it?
•     How many patients have you operated on and how are they doing?

Interstitial Cystitis - Finding the Right Physician for You

Patient Goals

    Patient goals include finding a physician 1) who is knowledgeable of and interested in treating IC, 2) who will provide an accurate diagnosis, appropriate treatments and ongoing care, and 3) who will educate you about treatment options, take time to listen, work collaboratively with you and respect the knowledge you have to share about your IC experience.


Why is this important?

    This is important because successfully managing a chronic illness like IC depends, in part, on your choice of physician and the attributes that physician brings to the process. Effective treatments are enhanced by a knowledgeable, compassionate physician. A urologist is a physician who specializes in treating urinary conditions.


How to go about finding the right physician

    Gather names of physicians from IC patients, Interstitial Cystitis Association (ICA) volunteers and the Physician Registry, a national list, available from the ICA, of physicians who have indicated an interest in treating IC. Check board certification through the American Board of Medical Specialties at 800-776-CERT ( http://www.certifieddoctor.org ) or consult your local library. Be aware that some highly recommended physicians may not have an expertise in treating IC. Make an appointment to meet the doctor. Ask some of the general questions listed below. You don't have to agree to an exam or medical tests during the first visit. Ask yourself how you feel about this initial meeting and trust your feelings.

 

Suggested questions to ask your doctor

    General questions to ask at an initial appointment:

•     Would you tell me what Interstitial Cystitis is and what symptoms patients experience?
•     What medical tests are used to diagnose IC? What findings support the diagnosis?
•     What are the treatment options for IC? What determines which ones you recommend?
•     Are there lifestyle changes that might be important in managing the symptoms of IC?

    Specific questions to ask regarding diagnostic testing, treatment and management of IC:

•     Why are these tests necessary? What are the risks, discomforts and costs of these tests? When will the results be available? May I have a written copy of the test results?
•     What are my test results? What do they indicate? What is my exact diagnosis? What is that based on?
•     What are the benefits, possible side effects and risks of the treatment you are recommending?
•     How long do I need to follow this/these treatment(s) before I might expect to see some improvement?
•     If this treatment plan is not helpful, or only partially helpful, what other treatments would you consider? Ask your physician if it would be possible for him or her to provide you with a list of possible treatment options so that if one treatment does not work, you will be reassured that there are other options available to you.

    Also, remember to ask about possible side effects and instructions for taking prescribed medications.


You have the right as a patient to...

•     Change physicians, consult other physicians, and get other medical opinions.
•     Obtain your medical records.
•     Be given adequate information to make informed decisions and give informed consent.
•     Decline or refuse suggested diagnostic procedures and/or treatment options.
•     Seek information about your medical condition from other sources.
•     Seek other kinds of care and/or support, which may include nutritional advice, group support, participation in the ICA, psychological support, pain management, stress management, or more.
•     Receive supporting documentation required by agencies with which you may file disability claims.
•     Receive supporting documentation required by your insurance provider when care is denied.
•     Receive a timely response to telephone contacts.

    Exercising these rights should not subject you to disrespectful treatment, threats or denial of care.

Alternative Medicine and Interstitial Cystitis

Most IC patients, have tried, or have considered trying, some form of alternative therapy to help relieve IC symptoms. 

Known as alternative, complementary, nutriceutical, holistic, integrative, and various other titles, this form of treatment, a shift away from allopathic medicine (most Western medicine is based on the allopathic principle that a disease is treated by creating an environment in which the disease can no longer survive), is sweeping the country. Various types of alternative therapies have existed for centuries, and have been practiced in the US for many years. But within the past few years, many of these therapies have become "mainstream," and it is not uncommon to find rows of herbal remedies in pharmacies as well as supermarkets. Some physicians are now incorporating many of these treatments into their practices, and practitioners of alternative medicine are setting up shop in even the smallest of towns. Considered standard forms of medical treatment in most of Europe for many years, alternative therapies in the US marketplace are now booming.

Dietary Supplement Health and Education Act

One reason for this boom is that in 1993, when the US Food and Drug Administration (FDA) began legislation to impose stricter regulations on the herbal and supplement industry, a massive consumer letter-writing campaign pressured the FDA to tone down their legislation. This resulted in the Dietary Supplement Health and Education Act (DSHEA), signed in 1994. This guideline for supplements, which includes vitamins, minerals and herbs, requires no proof of efficacy, no proof of safety, and sets no standards for quality control of products labeled as supplements. Manufacturers cannot make claims that their products affect (cure, alleviate, diagnose, prevent) a disease (if a product did, it would have to undergo standard FDA clinical testing to determine its safety and effectiveness), but they can cleverly word the product packaging to grab the consumer's attention.

For example, typical wording differences between an over-the-counter (OTC) laxative medication and an alternative herbal treatment that is purported to help relieve constipation would be the following: the OTC, FDA-approved medication can call itself a laxative; the alternative preparation cannot. The OTC medication can state that the medication helps to relieve constipation; the alternative preparation can use phrases such as, "promotes regularity," or "promotes healthy bowel function." Also, should questions arise about a product, the burden of proving negative claims lies with the FDA, not the manufacturer of the product. In other countries with regulation of supplement products, the burden of proof lies in the hands of the manufacturer, and standards of herb quality and safety assessment are enforced by the government, similar to the way in which the FDA controls the quality of prescription and over-the-counter medications in this country. Since there is no quality control, supplements can vary in quality and strength from bottle to bottle, and batch to batch. The FDA is currently working to redefine the DSHEA.

How Safe are These Products for IC Patients?

The enactment of the DSHEA has not helped the FDA in its attempts to ban questionable alternative treatments, even ones like the herb ephedra (a natural form of ephedrine, that can cause IC symptoms to flare) which has been linked to serious medical complications, such as heart failure. In many cases, healthy people are using alternative therapies to promote health, not to cure disease. Alternative therapies may turn out to play an important role in preventive medicine. Since the cause or causes of IC are unknown, and since IC has a yet unexplained relationship to other conditions such as allergies, fibromyalgia, irritable bowel syndrome, and/or vulvodynia, caution should be used when considering any treatment, including alternative treatments.

Not enough is understood yet about the nature of interstitial cystitis. Many IC patients have been told by various practitioners of alternative therapies to boost their immune systems with preparations like echinacea and ginseng, yet many of these practitioners have never heard of IC. Since IC researchers are still debating the possible link between IC and an autoimmune response, it would be unwise for anyone with autoimmune symptoms to try to "boost", their immune systems even further. Scientifically defined categories for the various causes of IC have not been established, and most IC patients (and physicians) don't know the actual cause or effect of IC in their bodies. This becomes territory that is potentially dangerous to your health.

Urothelial cancer

Bladder cancer accounts for just under 5% of all cancers and just over 3% of cancer deaths. Risk factors include cigarette smoking, occupational exposure to the class of chemicals known as aromatic amines, bladder infestation with the parasite Schistosoma haematobium, especially common in Egypt and Tanzania, and the immunosuppressant drug cyclophosphamide. The sensitivity of the bladder to toxicity from a variety of chemicals is explained by concentration of toxins within the urinary tract.

Kidney cancer accounts for 1.6% of all cancers and nearly 2% of cancer deaths. Kidney cancers are of three types: nephroblastomas (Wilms' tumours), adenocarcinomas (hypernephromas) and transitional and squamous cell carcinomas of the renal pelvis. The first category are limited to childhood and are of unknown aetiology, with the exception of a few of genetic origin. The second type constitute the majority of cases, are commoner in Western Europe and North America than in Africa and Asia, and are slowly increasing in incidence. There is a weak association with cigarette smoking. The third type constitutes around 10% of cases. Risk factors include occupational exposure to the chemicals causing bladder cancer, phenacetin ingestion (in sufficient quantities to cause analgesic nephropathy) and smoking. The increased risk is small. However, Balkan nephropathy, a form of chronic interstitial renal disease endemic in villages in parts of Romania, Bulgaria, Bosnia, Croatia and Serbia, increases the risk of carcinoma of the renal pelvis several hundredfold. Toxins in the River Danube and genetic factors have been implicated as possible contributory factors.

Urothelial tumours affect 11000 men and women annually in England and Wales, and cause the death of 5300 people. Treatment with radiotherapy will cure 30% of patients but causes significant toxicity in 30%. We have developed non toxic chemotherapy programmes that are as effective as radiotherapy but without toxicity.

In a new study we will be examining the efficacy of a new gemcitabine based treatment programme.

In patients with relapsed bladder cancer we are about to start an investigation of liposomal packaged adriamycin, a treatment that we hope will have efficacy with minimal toxicity.

Urethra

The bladder empties via the urethra. 

There are differences between the male and female urethras both on the gross level and histologically. Both have a proximal transitional, an intermediate pseudostratified and a distal stratified squamous epithelium.

Female 

In the female, the urethra runs a short course (4-5 cm) from the bladder to its termination.
 
 The lining epithelium changes over its course from transitional to pseudostratified columnar and finally to stratified squamous. Small collections of mucus-secreting cells can be found. These are called glands of Littré, which are much more well-developed in the male. 
Also, at about the midpoint, a voluntary muscular sphincter is present. 
Between the skeletal muscle and the mucosa, there is an inner longitudinal and an outer circular layer of smooth muscle.

Male 

The male urethra consists of three segments, The prostatic urethra, the membranous urethra and the penile urethra. 
As the urethra leaves the bladder, it enters and traverses the prostate, where it is called the prostatic urethra. 
About midway through, there is an elevation on the posterior wall of the urethra. 
This is the verumontanum or colliculus seminalis. There are three openings on the verumontanum, a central blind ending prostatic utricle and two lateral ejaculatory ducts. 
This portion of the urethra is lined with transitional epithelium and is easily identified due to the presence of the prostate.

Beyond the prostatic urethra, the membranous urethra spans only about one cm. 
This is where the external sphincter is present. 
This skeletal muscle provides voluntary control to the otherwise involuntary urethral sphincter. 
This segment of the urethra is lined with pseudostratified columnar epithelium. 
The urethra continues as the penile, or spongy, urethra. 
The penile portion is located within the corpus spongiosum of the penis. 
The epithelium here is mostly pseudostratified columnar and many glands of Littré are present. 
The luminal lining changes to stratified squamous near the urethral terminus.

Urethroplasty is a surgical procedure dealing with the repair of a defect or injury over the walls of the urethra. 
This surgery is carried out simply to fix the scar tissue blockage pertaining to the urethra known as urethral stricture.

Bladder

The two ureters empty into the

bladder. 
The ureters enter the bladder posteriorly at oblique angles, thereby preventing reflux of urine. 
The bladder is also lined with a transitional epithelium. It also contains an extensive lamina propria and three layers of smooth muscle which run perpindicular to each other. 

In this distended (filled) bladder,

two of the smooth muscle layers are evident, and the transitional epithelium looks like stratified squamous. 

In an empty bladder, the epithelium appears much taller, and the many epithelial infoldings reflect the elasticity of this organ. 

Ureter

After urine leaves the kidney via the collecting tubules, the calyces and the renal pelvis, it enters the ureter. 

The ureter carries urine from the kidney to the bladder. It is lined with transitional epithelium that is usually 4-6 cells thick. 

A thick lamina propria is also present. 

The epithelial layer is supported by an internal longitudinal layer and an outer circular layer of smooth muscle. 

The lumen of the ureter is star shaped. 

This cross section shows these layers of the ureter. 
 

The transitional epthelium of the ureter can be better appreciated in this higher magnification view. 
 

Kidney - Excretory Portion

Collecting duct: 

As urine leaves the distal tubule, it enters the excretory portion of the uriniferous tubule, the collecting duct. 
The collecting ducts begin in the cortex as arched connecting tubules. (Some texts refer to these as the terminal part or "connecting segment" of the distal convoluted tubule, but histologically and embryologically they are part of the collecting duct.) 
These connecting tubules straighten out and join other connecting tubules at the medullary ray to form a collecting duct. 
The collecting ducts penetrate deep into the medulla.

The histological appearance of the collecting ducts is similar to the distal tubule: pale staining, low cuboidal cells. 
The nuclei are centrally located. In contrast to the distal tubule, though, the collecting duct has an extra cell type, the intercalated cell. 
This cell type is involved in acid-base balance, and it stains more darkly than the principal cells of the collecting duct. This micrograph of a medullary ray shows some differences:

Both the distal tubule and collecting duct are less acidophilic than the proximal tubule, but the nuclei of the collecting duct are more centrally located than the apically-bulging nuclei of the distal tubule. Intercalated cells are distinguishable in some normal preparations; however preparations such as this immunostain for ANF are often necessary to identify these cells.

Papillary Ducts: 

Also called the ducts of Bellini, these ducts are formed in the inner medulla where several collecting ducts merge. 

This cross-section shows that the cells of the papillary ducts are similar to those of the collecting duct, but somewhat taller. 

At the apex of a medullary pyramid (a renal papilla), several papillary ducts will open into a minor calyx.

Minor calyces: 

There are 7-10 minor calyces per kidney. These excretory passages are lined with transitional epithelium, as is evident in this micrograph.

Major calyces: 

Two or three minor calyces then merge as they move toward the hilum, forming a major calyx. 
There are 3-5 major calyces per kidney. 
These, too, are lined by transitional epithelium.

Renal pelvis: 

The system of minor calyces, major calyces, and the funnel-like passage leading to the ureter make up the renal pelvis. 
Covered by transitional epithelium, the renal pelvis is histologically almost identical to the ureter. 
The renal pelvis can be thought of as the dilated proximal end of the ureter.

Juxtaglomerular Apparatus

The distal tubule courses back to the renal corpuscle from which it originated, and in doing so, it runs adjacent to the vascular pole of the corpuscle, near the extraglomerular mesangium, the afferent arteriole, and the efferent arteriole. The cells of the distal tubule wall at this point become very narrow, and their nuclei appear to be clumped closely together. 

This micrograph shows a section of distal tubule as it undergoes this transition to clumped nuclei. 

The closely-packed nuclei cause this region to stain densely, which gives it the name macula densa. 

This micrograph shows an excellent macula densa. 

This structure functions to alert the afferent arteriole of changes in urine osmolality. 
The receptors in the arteriole, called the juxtaglomerular cells, the macula densa, the extraglomerular mesangium and perhaps the efferent arteriole comprise the juxtaglomerular apparatus. 

The juxtaglomerular cells in the afferent arteriole consist of specialized renin-secreting smooth muscle cells that sit within the adventitia. These cells are in very close physical approximation with the macula densa.

The macula densa becomes stimulated under five circumstances:

1. Low blood sodium
2. Low blood volume or pressure
3. Sympathetic stimulation of beta adrenergic receptor
4. Increases in angiotensin levels
5. Increased prostaglandin levels

When stimulated, the macula densa signals the juxtaglomerular cells to release renin into the circulation. 

This micrograph shows renin, stained brown, localized to the modified smooth muscle cells around the afferent arteriole. 

Renin converts angiotensin into angiotensin I which is further converted into angiotensin II. Angiotensin II increases blood pressure by constricting arerioles and by stimulating aldosterone secretion. 
Aldosterone acts on distal tubule cells to increase sodium and chloride absorbtion. 
Water follows those ions out of the distal tubule and blood volume increases, thereby maintaining the blood pressure.

Distal Tubule

The kidney contains 1 - 4 million nephrons. 
The nephron is the functional unit of filtration. 
Each nephron has 4 main parts:

1. Renal Corpuscle, which can be further divided into a glomerulus and a Bowman's capsule
2. Proximal Tubule
3. Loop of Henle, with thin and thick limbs

4. Distal Tubule

From the distal convoluted tubule, the filtrate flows into a collecting duct. 
A nephron and the collecting duct which drains it are collectively called a uriniferous tubule. 

The ascending loop of Henle continues as the distal tubule, which is followed by the distal convoluted tubule. 
The distal tubule cells are simple cuboidal cells. 

They are generally much less eosinophilic than proximal tubule cells. 
Also, the lumen is not star shaped. 
The cells are smaller and flatter than proximal tubule cells so distal tubule cross sections appear to have larger lumens and more nuclei. 

The nuclei of distal tubule cells are more apical than those of the proximal tubule, and distal tubule nuclei often appear to bulge into the lumen. 
Because these cells contain no glycocalyx, no debris is visualized in the lumen. This micrograph illustrates some of these contrasting features of the distal and proximal tubules-- note that the distal tubule cells are flatter, the lumen is not star-shaped, there is no glycocalyx and no debris in the lumen.

Loop of Henle

The loop of Henle consists of the straight proximal tubule, the thin loop and the straight distal tubule. 

The straight proximal tubule (pars recta) comprises the descending thick segment and the straight distal tubule comprises the ascending thick segment.  
The thin loop cells are very low cuboidal and contain no brush border. 
They look similar to the capillaries which are often seen juxtaposed.

Although the thin loop cells are low cuboidal and the capillary cells are simple squamous, often the best way to distinguish the loop cells from the vascular endothelial cells is to look for red blood cells. If they are present then you have found a vessel.  
 

The length of the thin loop varies depending on the location of the nephron. 
Cortical loops only extend a short descending thin portion whereas juxtamedullary loops extend an extensive descending and ascending thin loop of Henle. 
 

The thick limb loop of Henle cells, which resemble proximal and distal tubule cells, from the capillaries. 
But deeper in the medulla, the loop cells are much thinner, and harder to distinguish from the capillaries.

Proximal Tubule

The proximal tubule consists of three histologically distinct parts, the S1, S2 and S3 segments.

These only roughly correspond with the appellations of proximal convoluted and proximal straight tubule (pars convoluta and pars recta). 

These appelations will not be discussed in depth here; it is sufficient to understand that the cells of the proximal tubule become shorter and less eosinophilic, and the tubule straightens out as it approaches the loop of Henle (the pars recta = the descending thick limb of the loop of Henle). 

Proximal tubule cells are simple cuboidal. 

They are also acidophilic due to a high content of long mitochondria concentrated in the base of the cell. 

They have a microvillous brush border that extends into the lumen of the nephron. 

The brush border is coated with a glycocalyx. In this PAS stained micrograph of the proximal convoluted tubule, the glycocalyx stains a reddish-pink. 

Localized along the basolateral membranes is the Na+/K+ ATPase, which pumps sodium out of the cells. 

On electron microscopy, or using special stains with light microscopy, apical vesicles and lysosomes can also be seen. 

This specially prepared LM shows lysosomal vesicles. 

Because the proximal tubule is the only section of the nephron involved in protein uptake, these vesicles can only be seen here. 

A good way to identify the proximal tubule by normal light microscopy is to determine the shape of the lumen. 

The lumen is star shaped and appears to contain debris (the glycocalyx) in most H&E sections. 

There are generally 5-7 cells per cross section.

Kidney: Nephron/Uriniferous Tubule

Each kidney contains 1-4 million nephrons. 

A nephron is the functional unit of filtration. 
Each nephron has 4 main parts:

Renal Corpuscle, which can be further divided into a glomerulus and a Bowman's capsule 

Renal plasma filtration begins in the glomerulus, which is situated within the renal corpuscle. 
The glomerulus is a ball of intermeshed network of highly fenestrated capillaries that protrude from the junction of the afferent and efferent arterioles. (This junction, where the afferent arteriole divides into several glomerular capillaries, is the vascular pole of the renal corpuscle, as seen in this micrograph.) 
The 50-100 nanometer fenestrae make up the first, least discriminating part of the filter of the renal corpuscle. 
The plasma filtrate leaves the glomerulus through those fenestrae. 
It should be noted that the glomerulus is made up of endothelial cells and mesangial cells. 
The rest of the renal corpuscle is made up of Bowman's capsule. 
Bowman's capsule consists of epithelial cells that envelop the glomerular capillaries and form the outer limit of the renal corpuscle. 
 

Those cells which surround the glomerulus make up the visceral layer and those that delimit the outer edge of Bowman's space comprise the parietal layer. This capsule surrounds the capsular space, the area into which the plasma is filtered. 
The point at which the parietal layer of Bowman's capsule becomes the proximal tubule is called the urinary pole of Bowman's capsule. 
This specially-stained micrograph shows the urinary pole of the capsule opening into the proximal tubule. 

The visceral layer epithelial cells are called podocytes (Gr. pod=foot). 
The podocytes extend a network of primary and secondary processes which end as pedicels out and around the glomerulus. 
Between the pedicels, there exist slits which are about 20 nanometers wide. 
These slits are covered by a slit diaphragm, which comprises a part of the renal corpuscle's filter. 
The slit diaphragm is made mostly of an anionic sialoprotein (podocalyxin). 
The filtrate enters Bowman's space through these slits and their diaphragm. 

At higher magnification, one can appreciate how the pedicels interdigitate to create the slit pores.


2. Proximal Tubule

3. Loop of Henle, with thin and thick limbs

4. Distal Tubule 

From the distal convoluted tubule, the filtrate flows into a collecting duct. 

A nephron and the collecting duct which drains it are collectively called a uriniferous tubule.

Renal Blood Flow - Kidney

About 25 % of one's total cardiac output goes to the kidneys to be filtered.

The summary of this flow is:
Aorta --> Renal artery --> interlobar artery --> arcuate artery --> interlobular artery --> afferent arteriole --> glomerular capillaries --> efferent arteriole -->
peritubular capillary plexus --> interlobular, arcuate, and interlobar veins

 
This photograph illustrates some of the larger vessels. 

At low power in a fetal kidney, the location of the arcuate vessels at the cortex/medulla border is evident. 
 

This vascular preparation shows afferent arterioles branching off an interlobular artery, then dividing into glomerular capillaries. 

The arterioles and glomerular capillaries will be discussed in greater detail later.

There are some other blood vessels present, like the stellate arteries found just beneath the capsule, and the vasa recta which nourish cells in the medulla.

Lobe/Lobule Lidney Concept

Another way to divide the kidney is into lobes and lobules. 
A lobe consists of a medullary pyramid and the cortex overlying it. Interlobar arteries and veins mark them off. 
 

The lobe can be divided into lobules, which consist of a medullary ray, the nephrons draining into it, and the section of the medullary pyramid continuous with it. In the cortex, interlobular arteries and veins mark them off, but there is no such clear division in the medulla. In this photograph, a lobe is outlined with a white line and a lobule with a black line. In this low power view of the cortex note that the interlobular vessels are not a part of the medullary rays.

Cortex and Medulla

The parenchyma of the kidney is divided into an outer cortex and an inner medulla. In a fresh, hemisected kidney, the cortex appears darker than the medulla, primarily because the cortex contains about 90% of the blood passing through the kidney. However, specimens with little or no blood can have a dark medulla and a lighter-colored cortex.

In the gross view, the cortex has a striated appearance. This series of vertical striations is known as medullary rays, because they appear to emanate from the medulla. Medullary rays consist of one or more collecting tubules, as well as the straight portion of the proximal tublules, distal tubules, and the loop of Henle. The medullary rays are surrounded by the rest of the cortical tissue: the renal corpuscles and the convoluted portions of the tubules. In this low power micrograph, medullary rays are quite evident, and at higher power, the main components of the medullary ray in the cortex can be compared: the collecting duct, distal tubule, and proximal tubule. These will be discussed further below.

The medulla consists of 10-18 pyramids. These pyramids are separated by inward extensions of cortical tissue called the renal columns of Bertin. One or two pyramids come together near the hilum, and drain into a minor calyx. (7-10 minor calyces per kidney.) These then gather into a major calyx (3-5 per kidney), which then joins the other major calyces to form the renal pelvis.