Advanced Pathophysiology Topics and Diabetic Nephropathy

This assignment provides in-depth information on advanced pathophysiology topics, specifically focusing on diagnostic tests for renal conditions such as urinalysis tests, and acid-base disorders like metabolic acidosis. It also delves into diabetic neuropathy, discussing the impact of high blood glucose levels on the glomerulus, leading to renal failure. The assignment includes detailed references from medical journals and books, providing a comprehensive understanding of these complex topics.

Running head: ADVANCED PATHOPHYSIOLOGY
ADVANCED PATHOPHYSIOLOGY
Name of the Student
Name of the university
Author’s note

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1. Diagnostic test or technique for a renal condition
A Urinalysis tests can be used for the presence of the protein and the blood in the urine. There
can be several reasons for the presence of protein in the urine. A urinalysis can be done for
assessing the color and the clearness. A urine infection may look the urine cloudy and foamy
urine may be a sign of kidney problems (Copstead &Banasik, 2013). Urine test can be done in
three parts such as visual exams that can be determined by the color and the clearness of the
urine. In a dipstick test a plastic strip with biomarkers can be dipped in urine and clinical
conditions are assessed by the change in the color of the stick. Urinalysis can also be used to
measure the level of acidity in the urine as high pH may indicate towards kidney stones or
infections. Glucose level in urine may indicate towards diabetes. Bilirubin, which is a waste
product, is removed from the liver and its presence in the urine can be a sign of liver disease.
Microscopic exams can be done for the detecting the leukocytes, erythrocytes, pathogens such
as bacteria and yeasts, tube shaped proteins known as the casts and presence of crystals
indicating kidney stones. The specific gravity of the urine can be defined as the density
measurement and relative proportion of the dissolved solid in the urine. The normal specific
gravity of the urine should be between 1.005- 1.035. Low specific gravity in urine indicates
conditions like diabetes insipidus and high specific gravity refers to excessive water loss,
diabetes mellitus and adrenal abnormalities. Specific gravity can be determined by Refractometer
and urinometer (Lim, 2014).

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2. Diagnostic test or technique useful in the diagnosis of an acid base disorder
Metabolic acidosis is an acid base disorder that is caused when the body generates acids in
excess and occurs mainly when the kidneys cannot remove the excess acids from the body. Some
of the causes of the metabolic acidosis includes kidney diseases (proximal renal tubular
acidosis), medicine poisoning due to aspirin or methanol or severe dehydration. Measurement of
metabolic acidosis can be done by the simultaneous measurement of the serum electrolytes as
well as the arterial blood gases. If the pH goes under 7.35 and the bicarbonate levels are
decreased and becomes less than 24mmol/L, then metabolic acidemia occurs. Anion gap and the
delta gap calculation can be helpful in detecting metabolic alkalosis. The anion gap can be
obtained by subtracting the sum of the chloride and bicarbonate ions from the serum sodium
concentrations (Vichot & Rastegar, 2014). Elevation of the anion gap values indicates metabolic
acidosis. The metabolic acidosis is categorized on the basis of, whether the anion gap is normal
or high. The delta gap is also measured in presence of metabolic acidosis for identifying the
metabolic alkalosis. The elevated anion gap is mainly caused for the presence of the compounds
that are negatively charged such as the ketones, sulphates, lactates, ethylene, and glycol (Vichot
& Rastegar, 2014). Acidemia due to the metabolic acidosis triggers hyperventilation decreases
the PaCo2. Serum anion gap is a useful diagnosis tool that can asses metabolic acidosis. No
change in the anion gap can be noticed in some disorders. The pattern of the anion gap
characterization helps not only in the diagnosis but also in the treatment. Augmentation of the
serum anion gap linked to the accumulation of the organic acid signifies the potential sources of
the bases (Kraut & Madias, 2012). Once the metabolic disturbance is cured, the accumulated
anions are converted in to equal amounts of bases and should be taken into consideration during
the treatment.

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3. Diabetic neuropathy and glomerular damage
Diabetic neuropathy is a significant reason of a chronic kidney disease and an end stage
renal failure. It is a common cause of renal failure globally. At first, there is a constriction of the
efferent arterioles and dilation of the afferent arterioles leading to hypertension and
hyperfiltration of the capillaries of the glomerulus (Lim, 2014). DN is mainly characterized by
the presence of lesions in the glomerulus and psthological presence of pathological amounts of
urine albumin. As a result, the glomerular filtration rate becomes less. The glomerular basement
thickens causing masangial expansion. Masangial expansion is the feature of diabetic
nephropathy and is related to the presence of proteinuria and hypertension (Cohen-Bucay &
Viswanathan, 2012).
The masangial expansion stimulates the compensatory mechanism for maintaining the
glomerular filtration by restricting the glomerular capillary filtration surface, which ultimately
leads to renal failure. Glomerular damage in patients with diabetic nephropathy is featured by
diffused expansion of the mesangial matrix. Another less common pattern of masangial
expansion can be seen in Kimmelstiel Wilson lesion. This condition is generally known as
glomeruloscelrosis(Cohen-Bucay & Viswanathan, 2012).
The high level of blood glucose level helps in the generation of the glycation end
products interfering with the turnover of the normal collagen, promoting matrix accumulation,
permeability of the vessels and the generation of the adhesion molecules. Urinary markers of the
damaged glomerulus are the augmented permeability of the plasma proteins such as albumin and
transferring (Cohen-Bucay & Viswanathan, 2012). This is secondary to factors such as loss of

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the charge selectivity of the glomerulus, loss of the size selectivity of the glomerulus and the
high intraglomerular pressure. Diagnostic methods include detection of high volumes of albumin
in urine. Ultimately, it results in renal failure and often mortality is caused by cardiovascular
failure.

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References
Cohen-Bucay, A., & Viswanathan, G. (2012). Urinary markers of glomerular injury in diabetic
nephropathy. International journal of nephrology, 2012.
Copstead, L. C., &Banasik, J. L (2013). Pathophysiology (5th ed.). St Louis, Missouri: Saunders
Elsevier.
Kraut, J. A., & Madias, N. E. (2012). Differential diagnosis of nongap metabolic acidosis: value
of a systematic approach. Clinical Journal of the American Society of Nephrology, 7(4),
671-679.
Lim, A. K. (2014). Diabetic nephropathy–complications and treatment. International journal of
nephrology and renovascular disease, 7, 361.
Vichot, A. A., & Rastegar, A. (2014). Use of anion gap in the evaluation of a patient with
metabolic acidosis. American Journal of Kidney Diseases, 64(4), 653-657.