7/25/2019 Lippin Cort Soft Notes Renal

1/3

A nephrotic syndrome is normally associated with 3 to 4+ proteinuria, fatty casts, oval fat

bodies, free fat droplets, and nonproliferative glomerulonephritis.

Typically, hematuria and red blood cell casts indicate a nephritic syndrome and

proliferative glomerulonephritis.

Chronic glomerulonephritis is characterized by proteinuria, variable hematuria, broad

way casts, and granular casts.

the patient!s neuromuscular dysfunction is most li"ely the result of hypo"alemia, the most

important and most serious side effect listed. #ypo"alemia is produced because the

diuretics cause a large amount of $a+ to collect in the distal tubules, which leads to $a+

reabsorption %sodium avidity& and a concomitant depletion of '+. This $a+('+ echangesite is a primary mechanism for renal control of '+ homeostasis.

)oststreptococcal glomerulonephritis is a relatively common complication of pharyngitis

in children * to years of age. -ost cases are caused by group A hemolyticstreptococci with specific types of - antigen.

The child!s puffiness is due to dramatically decreased glomerular filtration and the

resultant oliguria with salt and water retention. As with all cases of nephritis, there is

significant hematuria and proteinuria. The loss of protein combined with the salt andwater retention produces the characteristic edema, and the increased blood volume is

sufficient to eplain her modest hypertension.

Although systemic lupus erythematosus can be associated with glomerulonephritis, renalsymptoms characteristic of the nephrotic syndrome are more common in the early stages,

and it would be unusual for an /yearold to have lupus.

Acute tubular necrosis can be associated with water retention, edema, and high blood

pressure, but hematuria is not common in these patients. 0urthermore, most cases of acute

tubular necrosis are preceded by an identifiable ingestion of some acutely nephrotoicagent or ischemic damage secondary to shoc".

1uvenileonset diabetes fre2uently causes renal symptoms, but these changes are usually

nephrotic rather than nephritic in nature %i.e., lac" of hematuria and more substantialproteinuria&. The onset of diabetes is generally more gradual, and significant edema

would probably evolve over a longer period. 0inally, all cases of diabetes manifest with

polyuria, and salt and fluid retention are rarely seen prior to the onset of chronic renalfailure late in the disease. solated hyperaldosteronism is rare and not associated with

hematuria.

Almost 56 of $a+ is reabsorbed in the proimal tubular epithelium by several

processes, including active transport at the basolateral surface and cotransport of $a+ at

the luminal surface with glucose or amino acids. An additional 776 is reabsorbed by the

active transport process in the ascending thic" limb of the loop of #enle. The remaining

7/25/2019 Lippin Cort Soft Notes Renal

2/3

small percentage of $a+ that reaches the distal tubular epithelium is reabsorbed by a

highly regulated, aldosteronesensitive process involving echange with '+.

-embranous glomerulonephropathy %-8$& is depicted via hematoylin, eosin, and

methenamine silver stains and is characterized by the deposition of subepithelial immune

comple deposits %C9s&. :ubepithelial C9s may reduce the negative charge in theglomerular basement membrane %8;-& and inhen the disease progresses, the C9s become more

numerous and larger, leading to diffuse thic"ening of the 8;-. The glomerular reaction

to subepithelial C9s %i.e., by production of a new basement membrane around individualC9s& is represented on a silver stain %which stains the basement membrane& by spi"es

and later by domes and ?train trac"s.?

There are primary %/6& and secondary %76& forms of -8$. )rimary %renallimited& -8$ is caused by 8;-(podocyte autoantibodies and is associated with

eclusive subepithelial C9s that contain g8 and complement system protein, C3. nsecondary forms of -8$, the glomerular disorder occurs in association with an

etrarenal disease %e.g., lupus, malignant neoplasm, chronic viral hepatitis ;, and drug

reactions&. Affected glomeruli have a predominance of subepithelial C9s but may alsohave smaller numbers of mesangial or subendothelial C9s= the C9s may contain

immunoglobulin classes other than g8 as well as both early classical %C2, C4& and

alternative pathway %properdin& complement proteins %?full house? pattern by

immunofluorescence microscopy&.

The "idneys are especially sensitive to hypovolemic shoc" that lasts 3 minutes to hour.

Acute tubular necrosis is the most common "idney lesion seen in patients recoveringfrom hypovolemic shoc", and hyperal"emia 2uic"ly ensues, primarily as a result of

oliguria. n the absence of a substantial eternal potassium load, most patients have only

modest potassium accumulation, with rises in serum potassium of about .4 m- in a 74hour period. As with all causes of "idney failure, serum ;@$ and creatinine are mar"edly

elevated %creatinine as high as / to 7= normal ./ to .5&.

A positive A:B titer is generally ade2uate evidence to demonstrate a recent streptococcalinfection and is especially useful in diagnosing acute rheumatic fever as well as

poststreptococcal glomerulonephritis.

A complete blood count provides information that may be important in diagnosing

infection, anemia, or neoplasia.

The glomerular filtration rate %80& is "ept within a narrow range despite changes in

arterial blood pressure by a specialized tubuloglomerular feedbac" mechanism. This

mechanism is implemented by a special anatomic structure called the

7/25/2019 Lippin Cort Soft Notes Renal

3/3

tubule and