Case Report on Patient Anna
by Aaron Buchsbaum
(responses to assigned questions)

1.) One diagnosis we considered, found in Roy and Tscheschlog (1998), was cavernous sinus thrombosis, a specific type of facial edema.  While I never thought of this condition as a serious possibility, it seemed to correlate somewhat with a few symptoms the patient was feeling, including headache, nausea and fatigue (Roy and Tscheschlog 1998). There was more happening in the patient than could be explained by this condition, and several key symptoms, including eye pain and eye protrusion, were not apparent.  Researching this possibility did prove useful, however, as we found that facial edema could result from renal disorders (where fluid retention stems from lack of urine excretion), as well as cardiac and hepatic disorders (Roy and Tscheschlog 1998).

            A second consideration was a postrenal obstruction, which may have been responsible for low urine output (Fauci 1998).  According to DeGown and Brown (2000), postrenal obstructions are also responsible for a high BUN, which the patient exhibited.  BUN stands for blood urea nitrogen, where urea is a nitrogenous waste product excreted in urine.  Thus a high BUN indicates reduced kidney activity, as waste products are not being properly excreted and are instead collecting in the blood. This process of waste retention in the blood is known as azotemia (Fauci 1998).  Normal BUN is between 8-25 mg/dl (DeGown and Brown 2000), but our patient's was an astounding 135 mg/dl on admission day.  Postrenal obstruction was dismissed primarily for a lack of enlarged (distended) or painful kidneys, stemming from urine backup (Cotran, Kumar and Collins 1999).

            The other possibility our team considered was acute renal failure (ARF).  Renal failure is a condition where kidney function is disrupted, again causing retention of waste products in the blood (Merck Manual 2001).  ARF can be diagnosed in cases where there is a rapid decline in the functional capacity of the kidneys, as when urine output is suddenly decreased.  Causes include blockage of the ureters or urethra (where urine is effectively backed-up into the kidneys--see diagram below), decreased blood supply to the kidneys, or direct kidney injuries.  Again, results of this condition include elevated BUN levels as well as serum creatinine levels (Merck Manual 2001).  We felt that while acute renal failure could be used to describe Anna's condition, it was not specific enough.  We wanted to identify a clear direct cause and effect. 

 

 

 

 

 

2.) Our final diagnosis was poststreptococcal glomerulonephritis, a specific form of nephritis (medlineplus.gov 2001).  Nephritis is described in the Merck Manual as the inflammation of part or parts of the kidneys--for instance the glomeruli could be inflamed, preventing proper release of blood into nephrons.  We believe this is precisely the case with our patient.

As with other renal conditions nephritis results in aspects of azotemia, including high BUN and serum creatinine levels.  Symptoms also include edema, low urine output, blood in urine, and high blood pressure (hypertension) (Merck Manual 2001).  Anna exhibited all of these symptoms, making nephritis a strong possibility.  What clinched the diagnosis, however, was an immunofluorescence test showing a level of immune activity on Anna's kidneys (a). 

Robbin's Pathological Basis of Disease (Cotran, Kumar and Collins 1999) notes a type of nephritis known

as circulating immune complex nephritis, in which an abnormal immune reaction disrupts kidney function.

Antigen-antibody complexes (b) can actually coat the glomeruli of the kidneys, thus disrupting proper absorption of waste products (Merck Manual 2001).  In essence, the glomeruli are the places where waste products are dropped-off into the kidney--if these sites are blocked it is difficult for the waste to squeeze through, into the nephrons, to be filtered.  According to Robbins (Cotran, Kumar and Collins 1999), the antibodies give off what are known as "complements" which function to attack the invading antigen (Goldsby, Kindt and Osborne 2001).  However, when these complexes appear on glomeruli, there is the possibility that the complement will be produced directly into the basement membrane of the kidney, and attack normal kidney cells (Goldsby, Kindt and Osborne 2001).  This process, needless to say, can be extremely harmful, and potentially fatal, both to the kidneys and the patient.

3.) As stated before, BUN stands for blood urea nitrogen (DeGown and Brown 2000), and is described in many texts as an important factor in determining kidney malfunction.  Since urea is a nitrogenous waste product, normally filtered and excreted via healthy kidneys and urinary tracts, a high BUN shows that the kidney is unable to process the urea (DeGown and Brown 2000).  Thus, there is an abnormal amount of this waste product flowing through the blood.  In Anna's case, the antigen-antibody complexes were the reason for her high BUN; The coating of complexes shown by immunofluorescence effectively blocked fluid from leaving the normally porous glomeruli, instead remaining in the blood stream. 

            Creatinine is also a waste product, formed as a byproduct of protein metabolism (www.graylab.ac.uk 2001).  According to the National Library of Medicine (www.nlm.gov 2001), creatinine is specifically formed during conversion of ATP into creatine.  Like urea, creatinine excreted during normal kidney function.

4.) Medlineplus.gov, a subsidiary of the National Library of Medicine, states a high anti-streptolysin O titer indicates the presence of streptococci antibodies (2001).  Thus a high titer could indicate a streptococci infection, leading to such maladies as strep throat, post-streptococcal glomerulonephritis (another name for circulating immune complex nephritis), as well as scarlet fever and rheumatic fever (medlineplus.gov).  Our patient had no fever, so the latter two were quickly dismissed.  Anna did complain of a sore throat--likely stemming from the streptococci infection--but the real problem revolved around her kidneys, making the second disease a strong possibility.

5.)

            Shown above is an outline of how nephrons, the actual blood-filters in the kidneys, function under normal circumstances.  Water and solutes in the blood stream are forced out of the porous glomeruli and enter bowman's space (Starr and McMillan 2001), which serves a collection chamber for the soon-to-be-processed filtrate.  Pressure in the glomeruli is higher than in most capillaries, because the relatively large amount of blood delivered through the afferent (entering) arteriole must be pushed into the tiny glomeruli (Starr and McMillan 2001).  This controlled hypertension forces is important in forcing out filtrate.

            Many of the solutes--salt and glucose being prime examples--and water that are passed into the nephron are not intended for excretion; were this the case the body would quickly become depleted of these substances.  Instead, hormones such as antidiuretic hormone (ADH) and aldesterone make sure necessary amounts of water and solutes are passed back into the bloodstream-- in fact, about 99% of filtered water and salt is reabsorbed each day.  Peritubular capillaries, which weave around the nephronic pathway, bring these reabsorbed substances back into the bloodstream.  However, too much reabsorption (conversely, not enough excretion) can lead to harmful conditions such as hypertension, where blood pressure is raised due to sodium and water retention (Starr and McMillan 2001).  Such was the case with Anna.

            Secretion is the opposite of reabsorption, as substances from the peritubular capillaries are diffused into the nephronic pathway.  This is an important process by which blood pH is maintained, due to secretion of excess H⁺ ions that would otherwise acidify blood.  In normal kidney function secreted H⁺ ions (produced in various cellular processes) reacts with a buffer compound called bicarbonate inside the nephron, producing reaction produces water and carbon dioxide.  The water may be secreted as is necessary, while the CO₂ is returned to the blood, and eventually exhaled through the lungs (Starr and McMillan 2001).  Anna initially exhibited both a low blood level of CO₂ and a low (acidic) blood pH, which indicated an insufficient buffering of H⁺ atoms.  Bicarbonate was not able to enter her nephrons, due to the blockage of glomeruli from antibody-antigen complexes, preventing the formation CO₂ and allowing abnormal amounts of H⁺ into her bloodstream.

6.) Fischbach (2000) says that the yellow color of urine is derived from a pigment called urochrome.  Urochrome is a product of cell metabolism and is normally produced at a constant rate.  I believe that water intake, and subsequent urine concentration, plays a major part in determining how evident the urochrome is.  For instance a very concentrated urine, from which most of the water has been reabsorbed, would appear yellow.  On the other hand a well-hydrated person may produce clearer urine, owing to excess water excreted in the urine.

7.) Cotran, Kumar and Collins (1999) state that kidneys produce antihypertensive substances during normal function.  Some affect dilation of blood vessels directly, while others regulate sodium levels within the body.  In Anna's case, the latter is likely more important.  Most sodium is excreted from the nephronic pathway, however the small amount that does end up in urine is pivotal in maintaining homeostasis.  As sodium is excreted, especially in the loop of Henle, water diffuses out with it because of a shift in the concentration gradient (Starr and McMillan 2001).  In kidney problems where too much sodium is being excreted, it follows that too much water ends up back in the blood stream.  In a severe case like Anna's, where very little is entering the kidneys in the first place, sodium and water are both being retained in abnormally high amounts.  The end result is a raised blood pressure, due to over-filling of the blood vessels (Cotran, Kumar and Collin 1999).  That is to say, there is an excess of fluid in the blood stream, which exerts pressure on the blood vessels through which it travels-- for the blood vessels are not large enough to comfortably support the retained water and salts.

8.) Immune complexes form when antibodies effectively attach themselves to harmful antigens (see previous diagram) (Goldsby, Kindt and Osborne 2001).  The antibodies release molecules known as components, which attract neutrophils to the site of the immune complex (Fauci 1998).  In some cases, as in post-streptococcal glomerulonephritis, these complexes actually become attached to a basement membrane (Goldsby, Kindt and Osborne 2001).  In this case, the neutrophils are unable to isolate and completely surround the complexes, and can damage the basement membrane with released enzymes (Goldsby, Kindt and Osborne 2001).  As cells of the basement membranes are destroyed, more phagocytes are called upon to clean them up, thus creating a crowded locality of phagocytes, complexes, and dead cells.

9.) The kidney biopsy was pivotal in the formulation of our diagnosis.  Analyzing Anna's kidney tissue with immunofluorescence revealed the presence of antibody-antigen complexes.  Combined with a high anti-streptolysin O titer (indicative of an active streptococcal infection), cocci chains on her foot ulcer, and the likelihood that her brother had strep throat, we were able to make a confident diagnosis.  We conclude this patient has poststreptococcal glomerulonephritis, a condition where streptococcal immune complexes had disrupted proper kidney function.

10.) We knew Anna had to go on dialysis, as her kidneys were unable to maintain homeostasis.  As the Merck Manual (2001) suggests, we administered diuretics for excretion and to reduce edema.  As well, we started Anna on a low sodium diet in order to maintain a healthy water-sodium balance (Cotran, Kumar and Collins 1999).  This diet is designed to halt edema and excess fluid retention, as well as lower blood pressure through the removal of excess water from tissue.  Protein intake was also monitored, in an effort to control serum levels of creatinine, a product of protein metabolism (www.graylab.ac.uk).  Antihypertensive drugs were prescribed as well (medlineplus.gov).

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