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Renal failure is initiated by an initial pathology that has affected and continues to affect one or more structures of the nephron, to which certain adaptive injury mechanisms must be added.
The most important diseases that can induce chronic kidney disease and subsequently kidney function failure (incidence rates in brackets) are:
The irreversible destruction of the nephron population makes the elimination of solutes (residual products of metabolism) in the kidney insufficient.
The reduction in the rate of progression depends on the type of pathology that initiated it, but especially on the earliest therapy applied.
Nephron units that are still anatomically and/or functionally intact ‘hyperfunction’ to compensate, as far as possible, for an altered and no longer constant biochemistry of the organism.
As the number of inefficient nephrons progresses, the glomerular filtrate value (expressed as creatinine clearance) decreases, while creatininemia increases (normal values: 0.8-1.12 mg/dl).
Chronic renal insufficiency induces in the body, progressively and in a linear fashion, a loss of normal balance with important repercussions, such as the retention of residual products of protein metabolism (urea, uric acid, creatinine, etc.), the change in acid-base balance, water-salt retention and the reduced elimination and production of certain hormones.
This trend must be carefully monitored with frequent laboratory investigations.
When certain attempts at compensation, despite dietary and pharmacological treatments, no longer prove effective (the renal disease meanwhile continues!) at eliminating all or part of the substances derived from a profoundly altered metabolism, then the clinical signs and symptoms begin to appear that altogether realise the picture defined as uremia or ESDR (End Stage Disease Renal).
At this point, the time has come for replacement (dialysis and transplantation).
From what has been said, it follows that the pathological involvement of renal tissue is subtle, produces blurred clinical pictures even for years and generally, at least in the early stages, does not worry the patient and, unfortunately, neither do some physicians.
This can be distinguished and described, according to a progressive timing, in five stages.
Early diagnosis is not easy in nephrology!
In addition to the progressive reduction in renal function, a link to a significant and important cardiovascular morbidity and mortality favoured by chronic kidney disease itself has also been documented in recent years.
The concept of the aggressive and therefore aggravating role played by cardiovascular risk factors that are almost always present even when not causal (hypertension, diabetes, dyslipidaemia) is emphasised.
The study of urinary proteins constitutes a valuable marker of ongoing pathology, but at the same time they represent a risk factor for morbidity and mortality.
In light of these considerations, the importance of laboratory data for studying individual altered systems and disease evolution emerges.
There is no need to mention the urine test, which is irreplaceable, valuable and low-cost for the detection, verification or exclusion of many forms of morbidity.
This laboratory examination provides so much information, including the functioning of the kidneys and the detection of renal or extra-renal pathologies, to be verified by other investigations.
It is often necessary to collect 24-hour urine in order to carry out some important investigations (study of proteins, electrolytes, etc.).
In conclusion, individuals with chronic renal insufficiency do not complain of disorders except in the terminal or uremic phases, but it is only the laboratory that early on ‘condemns’ them with the associated profound changes in the body.
The results of the laboratory therefore have a non-substitutable function, and the therapeutic approach (lifestyle and medication) must be based on this data, in order to postpone the replacement phase (dialysis and transplantation) even by many years.
Therapy focuses both on treating the disease that induced the kidney disease and on diet and drug therapy in order to slow down (not cure!) the reduction in kidney function.
The diet is essentially linked to the reduction of proteins, giving preference to those defined as ‘noble’, as they are not produced by the body and are contained in good percentages in fish and farm animals.
With the preventive and modulated reduction of protein intake, i.e. in relation to the reduction of kidney function, it was found that the damaging effect linked to hyperfiltration decreased and at the same time the decrease in kidney function slowed down.
Obviously, in addition to protein reduction, other foods must be ‘adjusted’ in quantity and quality, both for ‘renal control’ and for possible cerebro-cardio-vascular disease.
Medications help to slow down the progression of kidney damage. In particular, anti-hypertensive substances, such as ACE inhibitors or angiotensin II receptor antagonists, induce a good result due to their main action, which is to dilate the efferent arteriole of the glomerulus.
Some calcium channel blockers can be combined, as they have anti-hypertensive activity, but also an action on a ‘muscle’ that leads to a reduction in contraction at the glomerular level by reducing hyperfiltration.
Finally, it should not be forgotten that some extra-renal factors can further damage the kidney and contribute to faster progression to terminal renal failure.
This often involves ‘normalising’ elevated blood pressure (usually the same drugs acting at the glomerular level are sufficient), hyperuricemia, dyslipidaemia in its various presentations and altered calcium-phosphorus metabolism.
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29/10/2022